Migratory Rate Research Articles

MiR-3918 Inhibits Tumorigenesis of Glioma via Targeting EGFR to Regulate PI3K/AKT and ERK Pathways.

Increasing evidence has demonstrated the miRNAs' action in cancerogenesis and tumor progression. Here, we explored the role and underlying mechanism of miR-3918 during glioma malignancy. miR-3918 and EGFR expression was detected in glioma tissues and tissues by RT-qPCR. The proliferative and migratory rate of glioma cells was assessed through CCK8 and Scratch wound-healing migration assay. Xenograft tumor mouse models were established for in vivo verification. A series of bioinformatics analysis coupled with luciferase reporter assays verified the targeted binding between miR-3918 and EGFR. Expression analyses demonstrated that miR-3918 was poorly expressed in glioma tissues while EGFR abundantly expressed. MiR-3918 overexpression impaired the proliferative and migratory capacities of glioma cells by inactivating PI3K/AKT and ERK pathways. Meanwhile, miR-3918 overexpression also retarded the growth of glioma xenograft. Mechanically, miR-3918 targeted EGFF which was further validated by the correlation of miR-3918 and EGFR expression in glioma tissues. When overexpressed, EGFR can restore the inactivated PI3K/AKT and ERK pathways caused by miR-3918 and influence the glioma cell proliferation and migration. Our findings are the first report that miR-3918/EGFR axis arrested the tumorigenesis of glioma via regulating PI3K/AKT and ERK pathways.

Cincumol prevents malignant phenotype of colorectal cancer cell line HCT116 via inhibiting PI3K/AKT signaling in vitro.

Colorectal cancer (CRC) is a common human cancer along with higher incidence and mortality, and this study aimed to identify the effect of cincumol on CRC and its potential mechanisms. CRC cell line HCT116 was used as the material. Cell proliferation was evaluated by CCK-8 assay, and cell migration was detected by scratch test and Transwell assay. TUNEL staining assay was used to evaluate cell apoptosis. The expression of target genes was detected by qualitative real-time polymerase chain reaction and western blot assays. Cincumol significantly reduced the proliferative and migratory rate and enhanced apoptotic rate of HCT116 cells. Meanwhile, the elevated levels of RBUsuh, Nicd and Tace was also observed in cincumol-treated HCT116 cells. Moreover, our findings revealed that additional cincumol inhibited the expression of p-PI3K and p-AKT, suggesting the inhibition of PI3K/AKT signaling might be involved in the protective role of cincumol on the malignant phenotypes of CRC cells in vitro. Cincumol inhibited the malignant phenotypes of CRC cells in vitro through inactivating PI3K/AKT signaling, suggesting that cincumol might be a potential anti-CRC agent.

LncRNA MORT negatively regulates FGF1 to suppress malignant progression of breast cancer.

To explore the biological function of long non-coding RNA (lncRNA) MORT in the malignant progression of breast cancer (BCa) and the underlying mechanism, and to provide a novel strategy for clinical treatment. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was conducted to detect differential level of MORT in BCa specimens and cell lines. The correlation between MORT level and pathological indexes of BCa patients was analyzed. After intervening MORT level in SKBR-3 and MCF-7 cells, cell viability, migratory rate and wound closure were examined through Cell Counting Kit-8 (CCK-8), transwell and wound healing assay, respectively. Dual-Luciferase reporter assay and rescue experiments were conducted to uncover the regulatory effect of MORT on its target gene FGF1. In vivo function of MORT in mediating tumor growth of BCa was finally assessed by generating a xenograft model in nude mice. MORT was downregulated in BCa tissues and cell lines. Low level of MORT predicted higher rate of distant metastasis in BCa patients. Overexpression of MORT in SKBR-3 cells reduced proliferative and migratory rates, while knockdown of MORT in MCF-7 enhanced them. Moreover, in vivo overexpression of MORT slowed down tumor growth of BCa in nude mice. MORT could negatively regulate its target gene FGF1, which was responsible for the anti-cancer role of MORT in BCa progression. MORT is downregulated in BCa specimens, which suppresses proliferative and migratory potentials of BCa cells by negatively regulating FGF1. MORT can be an effective target for precision treatment of BCa.

Requirement of Histone Deacetylase 6 for Interleukin-6 Induced Epithelial-Mesenchymal Transition, Proliferation, and Migration of Peritoneal Mesothelial Cells.

Aims: Influenced by microenvironment, human peritoneal mesothelial cells (HPMCs) acquired fibrotic phenotype, which was identified as the protagonist for peritoneal fibrosis. In this study, we examined the role of histone deacetylase 6 (HDAC6) for interleukin-6 (IL-6) induced epithelial-mesenchymal transition (EMT), proliferation, and migration of HPMCs.Methods: The role of HDAC6 in IL-6-elicited EMT of HPMCs was tested by morphological observation of light microscope, immunoblotting, and immune-fluorescence assay; and the function of HDAC6 in proliferation and migration of HPMCs was examined by CCK-8 assay, wound healing experiment, and immunoblotting.Results: IL-6 stimulation significantly increased the expression of HDAC6. Treatment with tubastatin A (TA), a highly selective HDAC6 inhibitor, or silencing of HDAC6 with siRNA decreased the expression of HDAC6. Moreover, TA or HDAC6 siRNA suppressed IL-6-induced EMT, as evidenced by decreased expressions of α-SMA, Fibronectin, and collagen I and the preserved expression of E-cadherin in cultured HPMCs. Mechanistically, HDAC6 inhibition suppressed the expression of transforming growth factor β (TGFβ) receptor I (TGFβRI), phosphorylation of Smad3, secretion of connective tissue growth factor (CTGF), and transcription factor Snail. On the other hand, the pharmacological inhibition or genetic target of HDAC6 suppressed HPMCs proliferation, as evidenced by the decreased optical density of CCK-8 and the expressions of PCNA and Cyclin E. The migratory rate of HPMCs also decreased. Mechanistically, HDAC6 inhibition blocked the activation of JAK2 and STAT3.Conclusion: Our study illustrated that IL-6-induced HDAC6 not only regulated IL-6 itself downstream JAK2/STAT3 signaling but also co-activated the TGF-β/Smad3 signaling, leading to the change of the phenotype and mobility of HPMCs. HDAC6 could be a potential therapeutic target for the prevention and treatment of peritoneal fibrosis.

Wound Healing Potential of Rhodomyrtus tomentosa and its Bioactive Compounds- Rhodomyrtone

Aims: The present work was aimed to study the phytochemical composition of a crude ethanolic extract of Rhodomyrtus tomentosa [SERT], and the presence of rhodomyrtone and SERT's in vitro wound healing activity.
 Introduction: Rhodomyrtus tomentosa is native plant to southern and southeastern Asia, India, east to southern China, Taiwan, Philippines, and south to Malaysia. In the traditional Vietnamese, Chinese and Malaysia, all its part, including leaves, roots, buds, and fruits have been used. A need for a new source of wound healing agent is the call for the investigation of the potential of R. tomentosa as the source of health-promoting agent, specifically as a natural wound healing agent.
 Methodology: SERT was screen for its phytochemicals and the detection of rhodomyrtone using liquid chromatography–mass spectrometry, /Quadrupole time-of-flight [LC-MS/QTOF] analysis. Cell viability, cell proliferation, and migration assay were performed to examine the SERT effect's in vitro wound healing activity on human fibroblast cells [CRL-2522].
 Results: The phytochemical study showed the presence of saponins, flavonoids, tannins and steroid in the crude ethanolic extract. The LC-MS analysis of crude ethanolic extract of SERT showed presents of rhodomyrtone which is one of the major compounds in the extract. SERT exhibit proliferative and migratory rate in human fibroblast cells [CRL 2522] in dose-dependent manner, which supports wound healing process. Its bioactive compounds presented wound healing activities at 0.325 up to 2.5 µg/mL.
 Conclusion: Both SERT and rhodomyrtone portrayed in vitro wound healing activities. Further studies to elucidate the mechanism of action of SERT and rhodomyrtone is recommended.

Alpha and beta adrenergic receptors modulate keratinocyte migration.

Keratinocyte migration into skin wounds is the step of the healing process that correlates with the wound closure rate. Keratinocyte migration, and wound epithelialization are decreased when beta 2-adrenergic receptors (B2AR) are activated by 1 μM epinephrine/adrenaline, resulting in delayed wound healing in human and mouse skin. In the present study, we found paradoxically, that in a subset of keratinocyte strains exposure to low concentrations of epinephrine (0.1 nM) increased, rather than decreased, their migratory rate. We find that both the alpha- and the beta-adrenergic receptors are expressed in human keratinocytes, and expression of alpha-2 AR subtypes demonstrated for the first time. Therefore, we tested if the alpha-AR could be modulating the increased migratory response observed in these cell strains. By using specific inhibitors to alpha-AR, we demonstrated that blocking A2B-AR could reverse the rapid cell migration induced by the 0.1 nM epinephrine. Phosphorylation of ERK was elevated after 1–10 minutes of the low epinephrine treatment and the A2B-AR inhibitor blocked the ERK phosphorylation. The results suggest that both the A2B-AR and B2AR mediate keratinocyte migration, in which with a low level of epinephrine treatment, A2B-AR could alter the B2AR signals and regulate the migration rate.

Abstract 2520: miRNAs with potential application for diagnosis, prognosis and treatment response prediction in uterine smooth muscle tumors

Abstract Background: miRNAs act as regulatory molecules at the post-transcriptional level. Their expression can influence in carcinogenesis, leading to alterations in the genetic and the epigenetic processes that contribute to tumors heterogeneous behaviors. miRNAs represent new potential biomarkers and promising translational targets in neoplasms therapy. These molecules expression has a crucial role in smooth muscle differentiation from mesenchymal stem cells. Leiomyoma (LM) is the most frequent benign uterine smooth muscle tumors (USMT), occurring in up to 80% of reproductive-age women. Leiomyosarcoma (LMS) is a malignant USMT that represents 40-60% of all gynecological sarcomas. This study aims to evaluate the expression profile and the role of miR-34a and miR-181b in LM and LMS cells. Methods: LM (THESCs CRL-4003) and LMS (SK-UT-1) cell lines were grown in specific mediums and conditions (ATCC recommendations). Cell lines were transfected with synthetic miRNA mimics and inhibitors of miR-34a and miR-181b and evaluated for proliferation, migration and gene expression (qPCR) assays. For gene expression analysis in patients' samples, 10 myometrium (MM), 10 LM and 15 LMS were selected and compared to cell lines expression profile. In silico analysis was performed to identify miR-34a and 181b main genetic interactions network of (MirtarBase database). Results: LM cells depicted higher basal expression levels of miR-34a and miR-181b, while the LMS presented a lower expression, both compared to MM. The same profile was observed for patients' samples. The 34a mimic showed great efficiency in expression induction at 24 h, in LM and LMS cells. Its inhibitor showed better efficacy at 72h in LM and 24 - 48h in LMS. For 181b, higher mimics efficiency was obtained at 72 and 96h in LM, and 24 and 48h in LMS. Its higher inhibition was observed at 24h, both for LM and LMS. LM cell proliferation showed a significant reduction for both mimics miRNAs at 72 and 96h, while inhibitory miRNAs decreased its proliferative capacity at 48 and 72h for 34a and only at 48h for 181b. Proliferation of LMS cells was lower only for 34a mimics at 72 and 96h and trended lower at 120h. Cell proliferation was lower when 181b was inhibited, at 72 and 96h, but a tendency was also observed at 48 and 120h. These preliminary results demonstrate a decreasing migratory rate in LM and LMS cells for 34a mimic and 181b inhibitor. In silico analysis depicted a strong interaction of the 34a, TP53 and BCL2 genes, and of the 181b, BCL2 and TIMP3. In conclusion, the upregulation of miR-34a and miR-181b induced cell proliferation and migration decrease in LM. For LMS cells, 34a upregulation was associated with the inhibition of cell proliferation and migration, while its downregulation induces the reduction of only the cell proliferation. miR-181b inhibition had an inductor effect over the LMS cells proliferation, but diminished in the cell migration. Citation Format: Bruna C. de Almeida, Isabela S. Faria, Laura G. Dos Anjos, Giovana N. Maffazioli, Edmund C. Baracat, Katia C. Carvalho. miRNAs with potential application for diagnosis, prognosis and treatment response prediction in uterine smooth muscle tumors [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 2520.

Comparative study of prostate cancer biophysical and migratory characteristics via iterative mechanoelectrical properties (iMEP) and standard migration assays

This study reveals a new microfluidic biosensor consisting of a multi-constriction microfluidic device with embedded electrodes for measuring the biophysical attributes of single cells. The biosensing platform called the iterative mechano-electrical properties (iMEP) analyzer captures electronic records of biomechanical and bioelectrical properties of cells. The iMEP assay is used in conjunction with standard migration assays, such as chemotaxis-based Boyden chamber and scratch wound healing assays, to evaluate the migratory behavior and biophysical properties of prostate cancer cells. The three cell lines evaluated in the study each represent a stage in the standard progression of prostate cancer, while the fourth cell line serves as a normal/healthy counterpart. Neither the scratch assay nor the chemotaxis assay could fully differentiate the four cell lines. Furthermore, there was not a direct correlation between wound healing rate or the migratory rate with the cells’ metastatic potential. However, the iMEP assay, through its multiparametric dataset, could distinguish between all four cell line populations with p-value < 0.05. Further studies are needed to determine if iMEP signatures can be used for a wider range of human cells to assess the tumorigenicity of a cell population or the metastatic potential of cancer cells.

Effect of Pomegranate Green Tea Mouthwash in Orogranulocyte Migratory Rate in Gingivitis Patients

Introduction Good oral health is necessary to attain general health. The mildest and most common of the oral diseases which can progress to periodontitis if not treated is gingivitis. Chronic periodontitis is an inflammatory disease which affects the supporting structures of the teeth.1-3 Recentl

Serglycin activates pro-tumorigenic signaling and controls glioblastoma cell stemness, differentiation and invasive potential

Despite the functional role of serglycin as an intracellular proteoglycan, a variety of malignant cells depends on its expression and constitutive secretion to advance their aggressive behavior. Serglycin arose to be a biomarker for glioblastoma, which is the deadliest and most treatment-resistant form of brain tumor, but its role in this disease is not fully elucidated. In our study we suppressed the endogenous levels of serglycin in LN-18 glioblastoma cells to decipher its involvement in their malignant phenotype. Serglycin suppressed LN-18 (LN-18shSRGN) glioblastoma cells underwent astrocytic differentiation characterized by induced expression of GFAP, SPARCL-1 and SNAIL, with simultaneous loss of their stemness capacity. In particular, LN-18shSRGN cells presented decreased expression of glioma stem cell-related genes and ALDH1 activity, accompanied by reduced colony formation ability. Moreover, the suppression of serglycin in LN-18shSRGN cells retarded the proliferative and migratory rate, the invasive potential in vitro and the tumor burden in vivo. The lack of serglycin in LN-18shSRGN cells was followed by G2 arrest, with subsequent reduction of the expression of cell-cycle regulators. LN-18shSRGN cells also exhibited impaired expression and activity of proteolytic enzymes such as MMPs, TIMPs and uPA, both in vitro and in vivo. Moreover, suppression of serglycin in LN-18shSRGN cells eliminated the activation of pro-tumorigenic signal transduction. Of note, LN-18shSRGN cells displayed lower expression and secretion levels of IL-6, IL-8 and CXCR-2. Concomitant, serglycin suppressed LN-18shSRGN cells demonstrated repressed phosphorylation of ERK1/2, p38, SRC and STAT-3, which together with PI3K/AKT and IL-8/CXCR-2 signaling control LN-18 glioblastoma cell aggressiveness. Collectively, the absence of serglycin favors an astrocytic fate switch and a less aggressive phenotype, characterized by loss of pluripotency, block of the cell cycle, reduced ability for ECM proteolysis and pro-tumorigenic signaling attenuation.

Club cell protein 16 in sera from trauma patients modulates neutrophil migration and functionality via CXCR1 and CXCR2

BackgroundClub Cell protein (CC)16 correlates with lung injury and respiratory complications, which are in part triggered by polymorphonuclear leukocytes (PMNL) in severely traumatized patients (TP). CC16 exerts anti-inflammatory and immunosuppressive effects, however, its influence on PMNL functions after trauma is unknown. Here, we evaluated whether CC16 present in sera from TP could modify the biological functions of PMNL.MethodsSera from 16 severely injured TP without pneumonia (no P, n = 8) or with pneumonia (P, n = 8) were collected at admission to emergency department (ED) and 1 day prior pneumonia and pre-incubated with or without anti-CC16 antibody for CC16 neutralization. Samples from the equal post-injury days in the corresponding no P group were used. Neutrophils were isolated from healthy volunteers (HV, n = 5) and incubated with 20% of the serum medium from TP, respectively. In PMNL, CD62L, CD11b/CD18 and CD31 expression, migratory capacity, phagocytosis rate, oxidative burst and apoptosis were investigated. In isolated PMNL, CXCR1 and CXCR2 were neutralized before stimulation with CC16, and oxidative burst, phagocytosis and apoptosis were analyzed in neutrophils and their subsets.ResultsSerum from the P group enhanced significantly PMNL migration compared to no P group, while CC16-neutralization further increased the migratory rate of PMNL in both groups. CC16-neutralization increased significantly the expression of CD62L in the P group at ED. Oxidative burst was significantly increased in the P group vs. no P during the study period. CC16 seemed to have no influence on oxidative burst and phagocytosis in TP. However, in a more controlled study design, CC16 induced a significant increase of oxidative burst and a decrease of apoptosis of CD16+ granulocytes. These effects were markedly observed in mature CD16brightCD62Lbright and immune suppressive CD16brightCD62Ldim neutrophils. In mature subset, CXCR1 and CXCR2 neutralization diminished CC16-induced effects.ConclusionsCC16 in sera from multiply traumatized patients, notably of those with pneumonia, has significant effects on PMNL. The results suggest an association of CC16 with CXCR1 and CXCR2. Our data suggest that CC16 reduces the migratory capacity of PMNL and thus modulates their function in patients with respiratory complications after trauma.

MicroRNA-93-5p/IFNAR1 axis accelerates metastasis of endometrial carcinoma by activating the STAT3 pathway.

The aim of this study was to elucidate whether microRNA-93-5p/IFNAR1 axis promoted proliferative and metastatic changes of endometrial carcinoma (EC) cells by regulating the STAT3 signaling pathway. The expression of microRNA-93-5p in EC tissues and cells was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Western blot was conducted to detect the protein expression of IFNAR1 in EC cells. Chi-square test was used to analyze the relationship between microRNA-93-5p expression and pathological characteristics of EC patients. The negative control, microRNA-93-5p mimics, microRNA-93-5p inhibitor or IFNAR1 vector were transfected into EC cells. Moreover, the proliferative and migratory potentials of EC cells were determined by cell counting kit-8 (CCK-8) and transwell assay, respectively. MicroRNA-93-5p expression was significantly upregulated in EC tissues and cells. High expression of microRNA-93-5p indicated poor survival of EC patients. The microRNA-93-5p expression level was correlated with FIGO stage and lymph node metastasis of EC. Meanwhile, a negative correlation was found between microRNA-93-5p and IFNR1 in EC tissues. Furthermore, the overexpression of microRNA-93-5p remarkably increased the viability and migratory rate of EC cells, which were reversed by IFNR1 up-regulation. MicroRNA-93-5p/IFNAR1 axis accelerates metastasis of EC through the STAT3 pathway.

Pathobiological features favouring the intercontinental dissemination of highly pathogenic avian influenza virus.

Avian influenza viruses (AIVs) are a continued threat to global health and economy. Unlike other highly pathogenic AIVs, novel H5N8 disseminated very quickly from Korea to other areas in Asia, Europe and even North America following its first outbreak in 2014. However, the pathobiological features of the virus that favoured its global translocation remain unknown. In this study, we used a compartmental model to examine the avian epidemiological characteristics that would support the geographical spread of influenza by bird migration, and to provide recommendations for AIV surveillance in wild bird populations. We simulated virus transmission and translocation in a migratory bird population while varying four system properties: (i) contact transmission rate; (ii) infection recovery rate; (iii) mortality rate induced by infection; and (iv) migratory recovery rate. Using these simulations, we then calculated extinction and translocation probabilities for influenza during spring migration as a function of the altered properties. We find that lower infection recovery rates increase the likelihood of AIV translocation in migratory bird populations. In addition, lower mortality rates or migration recovery rates also favour translocation. Our results identify pathobiological features supporting AIV intercontinental dissemination risk and suggest that characteristic differences exist among H5N8 and other AIV subtypes that have not translocated as rapidly (e.g. H5N6 and H5N1).

ROCK Inhibitor Y27632 Induced Morphological Shift and Enhanced Neurite Outgrowth-Promoting Property of Olfactory Ensheathing Cells via YAP-Dependent Up-Regulation of L1-CAM.

Olfactory ensheathing cells (OECs) are heterogeneous in morphology, antigenic profiles and functions, and these OEC subpopulations have shown different outcomes following OEC transplantation for central nervous system (CNS) injuries. Morphologically, OECs are divided into two subpopulations, process-bearing (Schwann cells-like) and flattened (astrocytes-like) OECs, which could switch between each other and are affected by extracellular and intracellular factors. However, neither the relationship between the morphology and function of OECs nor their molecular mechanisms have been clarified. In the present study, we first investigated morphological and functional differences of OECs under different cytokine exposure conditions. It demonstrated that OECs mainly displayed a process-bearing shape under pro-inflammatory conditions (lipopolysaccharide, LPS), while they displayed a flattened shape under anti-inflammatory conditions [interleukin-4 (IL-4) and transforming growth factor-β1 (TGF-β1)]. The morphological changes were partially reversible and the Rho-associated coiled-coil-containing protein kinase (ROCK)/F-actin pathway was involved. Functionally, process-bearing OECs under pro-inflammatory conditions showed increased cellular metabolic activity and a higher migratory rate when compared with flattened OECs under anti-inflammatory conditions and significantly promoted neurite outgrowth and extension. Remarkably, the morphological shift towards process-bearing OECs induced by ROCK inhibitor Y27632 enhanced the neurite outgrowth-promoting property of OECs. Furthermore, as the downstream of the ROCK pathway, transcriptional co-activator Yes-associated protein (YAP) mediated morphological shift and enhanced the neurite outgrowth-promoting property of OECs through upregulating the expression of the neural adhesion molecule L1-CAM. Our data provided evidence that OECs with specific shapes correspond to specific functional phenotypes and opened new insights into the potential combination of OECs and small-molecule ROCK inhibitors for the regeneration of CNS injuries.

Migration and Nuptiality in Course of Revitalization the Economic Development of Yakutia

Over the period of semicentenial development the economic processes in Yakutia have been accompanied by large-scale migratory population movement. An active exploration of new territories resulted in migration to become a basic population change component substantially defining population age structure, birth and death rate in the region. The article considers the interrelation of migratory inflow and nuptiality changes in local territories of intensive economic development. The correlation analysis of time-series data is provided. The hypothesis is tested of existing one-year time log between a migrant arrival and wedding. It was discovered that the periods of intensified regional economic development accompanied by large-scale inflow of migrants, featured very high strength of relationship between the stream of arrivals and marriage registrations. In particular, Pearson’s pair correlation coefficient between the arrivals and marriages made up 0.885 in West Yakutia in 1960th, and 0.962 - in South Yakutia in 1970th. The revealed relationship was largely determined by a favorable proportion between the number of persons in marriable age among migrants and their commitment towards long stay in Yakutia, including their intentions to establish a family. The analysis of dynamic numbers has shown that the deep social and economic, political changes of the 1990th in the region were accompanied by radical change of migration vector and the increase in migratory seasonal component. These factors resulted in a considerably falling migratory rate, reduced or even discontinued interrelation between arrival rates and officially registered marriages.

LncRNA ATB promotes the proliferation and metastasis of lung cancer via activation of the p38 signaling pathway.

Long non-coding RNA (lncRNA) activated by TGF-β (ATB) has been reported to be widely expressed in different types of cancer; however, the function of ATB in lung cancer remains unclear. In order to elucidate the role of ATB in lung cancer, reverse transcription-quantitative polymerase chain reaction was used to detect the expression of ATB in tumor tissues and corresponding non-tumor lung tissues from 32 patients with lung cancer. Furthermore, the association between the expression of ATB and clinical characteristics was investigated. Cell proliferation was assessed using a cell counting kit-8 assay and cell migration was assessed using a wound healing assays. Epithelial-mesenchymal-transition and mitogen-activated protein kinase signaling pathway activity was examined using western blotting. It was demonstrated that ATB was highly expressed in lung cancer tissues compared with noncancerous tissues, and associated with tumor size and metastasis. It was also demonstrated that ATB was highly expressed in the lung cancer cell lines, A549 and HCC827, compared with the HBE-1 cell line. Suppression of ATB significantly inhibited the proliferation and migratory rate of lung cancer cells. The protein expression levels of p38, E-cadherin and N-cadherin were altered by suppression of ATB expression. Overall, the present study demonstrated that ATB may promote the development of lung cancer.

Variation in mercury concentration in juvenile Magellanic penguins during their migration path along the Southwest Atlantic Ocean

The vulnerability of seabirds related to their migratory dynamics is frequently linked to environmental problems along the migration path. In this context, Magellanic penguins (Sphenicus magellanicus) seem to be vulnerable to an extensive range of environmental disturbances during their northward migration along the Atlantic waters of South America, which include by catch, marine debris ingestion, overfishing and environmental contamination. In this study, we investigate mercury accumulation in muscle and hepatic tissues of juveniles penguins collected along the Brazilian coast during three migratory seasonal years (2006, 2008 and 2012) and three areas along a latitudinal gradient. We found significant differences in Hg levels across the years, with higher hepatic Hg levels found in tissues of penguins sampled in 2008. The higher Hg levels in samples of penguins from 2008 might be attributed to variations in body condition or Hg uptake, associated with the trophic imbalance linked to an extreme El Niño event during that year. Significant differences in Hg accumulation across the latitudinal areas were also observed. The penguins sampled at the farthest area from the breeding ground presented the higher levels of Hg and also the poorest body condition. Body condition and other traits may influence the levels of chemical pollutants and decrease the migratory success rate in the juvenile age phase, compromising population dynamics.

In Vitro Wound Healing Potential of Stem Extract of Alternanthera sessilis.

Impaired wound healing is one of the serious problems among the diabetic patients. Currently, available treatments are limited due to side effects and cost effectiveness. In line with that, we attempted to use a natural source to study its potential towards the wound healing process. Therefore, Alternanthera sessilis (A. sessilis), an edible and medicinal plant, was chosen as the target sample for the study. During this investigation, the wound closure properties using stem extract of A. sessilis were analyzed. Accordingly, we analyzed the extract on free radical scavenging capacity and the cell migration of two most prominent cell types on the skin, human dermal fibroblast (NHDF), keratinocytes (HaCaT), and diabetic human dermal fibroblast (HDF-D) to mimic the wound healing in diabetic patients. The bioactive compounds were identified using gas chromatography-mass spectrometry (GC-MS). We discovered that the analysis exhibited a remarkable antioxidant, proliferative, and migratory rate in NHDF, HaCaT, and HDF-D in dose-dependent manner, which supports wound healing process, due to the presence of wound healing associated phytocompounds such as Hexadecanoic acid. This study suggested that the stem extract of A. sessilis might be a potential therapeutic agent for skin wound healing, supporting its traditional medicinal uses.

Quantifying population size of migrant birds at stopover sites: Combining count data with stopover length estimated from stable isotope analysis

Abstract Regular counts of migrating animals at stopover sites have been used as a measure of site importance at the global scale as well as for monitoring long‐term population changes. However, migratory passage can last for several weeks and the turnover rate of individuals is often high, preventing the use of peak counts to estimate the total number of migrants. This estimate can be achieved, however, by combining count data with information on stopover length. Here, we developed a new method to quantify the total number of migrant birds using stopover areas hosting overlapping populations of local (breeding or wintering) and passage individuals of a given species. We illustrate the application of this method by estimating the number of spring migrant dunlins Calidris alpina stopping over at the Tagus estuary (Portugal). We used carbon and nitrogen isotopic signatures in toenails to identify migrants and to estimate their proportion in total counts. We then employed isotopic clock models to determine time since arrival (TSA) of individuals from signatures in red blood cells and plasma and, using a simulation approach, we derived the relationship between TSA and stopover length. Finally, by dividing the number of migrants.day (obtained from counts) by the stopover length, we assessed the size of the migrant population. We demonstrated that stopover length can be directly predicted from mean TSA values of birds sampled during migration, regardless of variations in (1) migratory rate, that is, the phenology of arrivals throughout the migratory period and (2) the number of birds involved in the migratory event. Migrant dunlins stayed on average 7.5 days at the Tagus estuary during spring migration, which combined with count data resulted in an estimate of c. 30,000 passage dunlins, using the study site. Our novel approach is not strict in its assumptions, and therefore can be customised to the specificities of different taxa and study areas. Estimates of total number of migrants along migratory flyways are critical to identify priority sites for conservation action. In fact, single stopover sites may host a very significant proportion of a global population albeit for a short period.

Magnetic resonance imaging of odorant activity-dependent migration of neural precursor cells and olfactory bulb growth

Neural progenitors or neuroblasts are produced by precursor cells in the subventricular zone (SVZ) and migrate along the rostral migratory stream (RMS) to the olfactory bulbs (OB) throughout life. In the OB, these adult born neurons either die or replace existing olfactory interneurons, playing a critical role in the stabilization of OB circuitry. Although several aspects of the addition of new neurons into the OB have been studied, it is unclear whether long-distance activity from the OB can regulate the influx of migrating neuroblasts along the RMS. In this study, iron oxide-assisted MRI was used to track the migration of neuroblasts in combination with reversible naris occlusion to manipulate odorant-induced activity. It was found that decreasing olfactory activity led to a decrease in the rate of neuroblast migration along the RMS. Removal of the naris occlusion led to an increase in migratory rate back to control levels, indicating that olfactory activity has regulatory function on neuroblast migration in the RMS. Blocking odorant activity also led to an arrest in OB growth and re-opening the block led to a rapid re-growth returning the bulb size to control levels. Furthermore, pharmacogenetic elimination of the neuroblasts demonstrated that they were required for re-growth of the bulb following sensory deprivation. Together, these results show that sensory activity, neural migration and OB growth are tightly coupled in an interdependent manner.