Induced Colony Formation Research Articles

Zymogen granule protein 16B (ZG16B) is a druggable epigenetic target to modulate the mammary extracellular matrix.

High tissue density of the mammary gland is considered a pro-tumorigenic factor, hence suppressing the stimuli that induce matrix buildup carries the potential for cancer interception. We found that in non-malignant mammary epithelial cells the combination of the chemopreventive agents bexarotene (Bex) and carvedilol (Carv) suppresses the zymogen granule protein 16B (ZG16B, PAUF) through an interaction of ARID1A with a proximal enhancer. Bex + Carv also reduced ZG16B levels invivo in normal breast tissue and MDA-MB231 tumor xenografts. The relevance of ZG16B is underscored by ongoing clinical trials targeting ZG16B in pancreatic cancers, but its role in breast cancer development is unclear. In immortalized mammary epithelial cells, secreted recombinant ZG16B stimulated mitogenic kinase phosphorylation, detachment and mesenchymal characteristics, and promoted proliferation, motility and clonogenic growth. Highly concerted induction of specific laminin, collagen and integrin isoforms indicated a shift in matrix properties toward increased density and cell-matrix interactions. Exogenous ZG16B alone blocked Bex + Carv-mediated control of cell growth and migration, and antagonized Bex + Carv-induced gene programs regulating cell adhesion and migration. In breast cancer cells ZG16B induced colony formation and anchorage-independent growth, and stimulated migration in a PI3K/Akt-dependent manner. In contrast, Bex + Carv inhibited colony formation, reduced Ki67 levels, ZG16B expression and glucose uptake in MDA-MB231 xenografts. These data establish ZG16B as a druggable pro-tumorigenic target in breast cell transformation and suggest a key role of the matrisome network in rexinoid-dependent antitumor activity.

Synergistic Effect of Saccharin and Caffeine on Antiproliferative Activity in Human Ovarian Carcinoma Ovcar-3 Cells.

The purpose of this study was to confirm the antiproliferative and apoptotic induction potential of a saccharin and caffeine combination in ovarian cancer cells. The cell line used was Ovcar-3, and the cell viability was measured through a WST-8 assay, while a Chou-Talalay assay was used to confirm the synergistic effect of saccharin and caffeine on the ovarian cancer cells. A clonogenic assay, annexin V-FITC/PI-PE double-staining, and RT-PCR were performed to confirm the expression of genes that induce colony formation, cell viability, and apoptosis in ovarian cancer cells treated with the saccharin-caffeine combination. It was demonstrated that both saccharin and caffeine decreased the viability of Ovcar-3 cells, and the cell viability decreased even more significantly when the cells were treated with the combination of saccharin and caffeine. The clonogenic assay results showed that the number of colonies decreased the most when saccharin and caffeine were combined, and the number of colonies also significantly decreased compared to the single-treatment groups. Based on flow cytometry analysis using annexin V-FITC/PI-PE double-staining, it was confirmed that the decrease in cell viability caused by the combination of saccharin and caffeine was correlated with the induction of apoptosis. The results of the RT-PCR confirmed that the combined treatment of saccharin and caffeine promoted cell apoptosis by regulating the expression of apoptosis-inducing genes. These results demonstrate that the combination of saccharin and caffeine more efficiently inhibits the proliferation of Ovcar-3 cells and induces apoptosis in vitro.

Grazing inhibition in Daphnia and Bosmina by colony formation of Desmodesmus subspicatus triggered by sodium octyl sulfate.

There are growing concerns that several aquatic contaminants can indirectly alter biological interactions by inhibiting the adaptive phenotypic plasticity of organisms, even at nonlethal concentrations. In Scenedesmaceae, a family of green algae, many chemicals interfere with defensive colony formation against grazers (i.e., through induced or limited coloniality). Although several studies have demonstrated that the effects of coloniality can limit the feeding capacity of Daphnia spp., grazing inhibition in other zooplankton species is not well understood. In this study, we examined the influence of sodium octyl sulfate (SOS) on the growth and morphology of Desmodesmus subspicatus and on the feeding rates of three cladoceran species (Daphnia galeata, Bosmina longirostris, and Bosmina fatalis) feeding on SOS-induced colonies under factorial conditions of different food levels and grazer ages. SOS remarkably induced colony formation with no observed effect on growth in D. subspicatus. D. galeata and B. fatalis showed a remarkable reduction in feeding rates when they fed on colonial D. subspicatus, whereas no significant effect of the prey morphotype was found on the feeding rates of B. longirostris. Microscopic observations of algal morphology after being grazed showed that each species can consume colonial prey depending on food level and age. Comparisons of the inhibition ratio of feeding among the three cladocerans revealed that Daphnia was more sensitive to prey coloniality compared with Bosmina. Our findings provide specific insights into the effects of chemically interfered colony formation on population dynamics and community structures.

Evodiamine impairs HIF1A histone lactylation to inhibit Sema3A-mediated angiogenesis and PD-L1 by inducing ferroptosis in prostate cancer

Prostate cancer (PCa) is among the most commonly diagnosed solid cancers in male adults. However, most anti-angiogenic therapies and immunotherapies fail to achieve durable remission in advanced PCa. Integrative analysis indicated that Sema3A was negatively correlated with the pathological malignancy and was involved in angiogenesis, cell adhesion, and immune infiltrates in PCa. Sema3A significantly inhibited vascular endothelial growth factor (VEGFA)-induced colony formation, cell proliferation, and PD-L1 expression in PCa cells. Network pharmacological analysis demonstrated that evodiamine, a natural alkaloid compound derived from Evodiae fructus fruits, might regulate Sema3A, lipid metabolism, and monocarboxylic acid transport signaling of PCa. Evodiamine evidently inhibited PCa cell viability in a time-dose-dependent manner. Furthermore, evodiamine impaired angiogenesis by increasing Sema3A expression, and induced ferroptosis by reducing glutathione peroxidase 4 (GPX4) expression, which could be reversed by the ferroptosis blocker ferrostatin-1. Lactate treatment increased hypoxia-inducible factor (HIF)-1α and PD-L1 expressions while restricting Sema3A expression in PCa cells, which could be reversed by silencing monocarboxylate transporter 4 (MCT4) expression. Moreover, evodiamine markedly blocked lactate-induced angiogenesis by restricting histone lactylation and expression of HIF1A in PCa cells, further enhancing Sema3A transcription while inhibiting that of PD-L1. In vivo, evodiamine remarkably inhibited PCa xenograft growth in nude mice, repressing expressions of HIF1α, H3K18la, GPX4, PD-L1, and proliferation, while hindering angiogenesis by increasing Sema3A expression. Therefore, Sema3A represents an essential antineoplastic biomarker, while evodiamine may act as a metabolic-epigenetic modulator, as well as a promising agent in either PCa anti-angiogenic therapy or immunotherapy.

Carbon nanoparticles induce DNA repair and PARP inhibitor resistance associated with nanozyme activity in cancer cells

BackgroundQuantum nanodots especially carbon nanoparticles (CNPs) have been widely studied in biomedicine in imaging, and drug delivery, but anti-cancer mechanisms remain elusive.MethodsHere, we investigated a type of cell death induced by food (beet, soybean) derived CNPs in cancer cells and tested whether CNPs induced DNA damage and resistant to anti-cancer agent PARP inhibitor (PARPi) could be overcome by quantum calculations, TEM, AFM, FT-IR, soft agar assay, and cytotoxicity assay.ResultsAt high doses, CNPs derived from beet lead to a pop-like apoptosis (Carbopoptosis) in cancer cells. Quantum mechanical calculations confirmed CNPs binding with phosphate groups as well as DNA bases. At low doses, CNPs develop PARPi drug resistance through interactions between CNPs and PARPi. A synergistic drug effect was achieved with the combination of phosphatase inhibitor (PPi), PARPi, and CNPs. This is corroborated by the fact that sulfur modulated CNPs which exhibit super high phosphatase nanozyme activity abrogated the CNPs induced colony formation in anchorage-independent cancer cell growth.ConclusionThus, our data suggest the CNPs intrinsic nanozyme activity of phosphatase may crosstalk with drug resistance, which can be reversed upon modulations.

Inhibition of LIFR Blocks Adiposity-Driven Endometrioid Endometrial Cancer Growth.

Endometrial cancer (EC) is the fourth most common cancer in women, and half of the endometrioid EC (EEC) cases are attributable to obesity. However, the underlying mechanism(s) of obesity-driven EEC remain(s) unclear. In this study, we examined whether LIF signaling plays a role in the obesity-driven progression of EEC. RNA-seq analysis of EEC cells stimulated by adipose conditioned medium (ADP-CM) showed upregulation of LIF/LIFR-mediated signaling pathways including JAK/STAT and interleukin pathways. Immunohistochemistry analysis of normal and EEC tissues collected from obese patients revealed that LIF expression is upregulated in EEC tissues compared to the normal endometrium. Treatment of both primary and established EEC cells with ADP-CM increased the expression of LIF and its receptor LIFR and enhanced proliferation of EEC cells. Treatment of EEC cells with the LIFR inhibitor EC359 abolished ADP-CM induced colony formation andcell viability and decreased growth of EEC organoids. Mechanistic studies using Western blotting, RT-qPCR and reporter assays confirmed that ADP-CM activated LIF/LIFR downstream signaling, which can be effectively attenuated by the addition of EC359. In xenograft assays, co-implantation of adipocytes significantly enhanced EEC xenograft tumor growth. Further, treatment with EC359 significantly attenuated adipocyte-induced EEC progression in vivo. Collectively, our data support the premise that LIF/LIFR signaling plays an important role in obesity-driven EEC progression and the LIFR inhibitor EC359 has the potential to suppress adipocyte-driven tumor progression.

HMGN4 plays a key role in STAT3-mediated oncogenesis of triple-negative breast cancer.

High-mobility group nucleosome-binding domain 4 (HMGN4) exerts biological functions by regulating gene transcription through binding with nucleosome. As a new epigenetic regulator discovered in 2001, its biological functions have not been clarified. HMGN4 belongs to HMGNs family, in which HMGN1, 2 and 5 have been reported to play roles in oncogenesis of various cancers. However, it is reported that HMGN4 was associated with thyroid and liver cancer. In this study, we discovered for the first time that HMGN4 was highly expressed in human triple-negative breast cancer (TNBC), based on the analysis of the TCGA database. Moreover, we found that HMGN4 controlled the proliferation of human TNBC cells both in vitro and in vivo. Mechanistically, the positive correlation occurred between HMGN4 and STAT3 downstream genes while HMGN4 played an indispensable role in constitutively active STAT3 (STAT3C) induced colony formation. Interestingly, we reported that STAT3 regulated HMGN4 transcription as its transcriptional factor by chromatin immunoprecipitation and HMGN4 promoter-luc assays. That is to say, there is a feed-forward signaling circuit between HMGN4 and STAT3, which might control TNBC cell growth. Finally, we proved that the interference of HMGN4 by nanovehicle-packaged siRNA may be a potentially effective approach in TNBC treatment. In summary, our findings not only identified a novel regulator in TNBC cell proliferation but also revealed the mechanism by which HMGN4 acted as a downstream gene of STAT3 to participate in the STAT3 pathway, which indicated that HMGN4 was likely to be a potential novel target for anti-TNBC therapy.

IL-36G promotes cancer-cell intrinsic hallmarks in human gastric cancer cells.

Interleukin-36 gamma (IL-36G) is a member of the IL-36 subfamily of cytokines and acts as a potent driver of inflammation. IL-36G has been extensively characterized in the pathogenesis of psoriasis and has been recently described to play roles in wound healing particularly in the gastrointestinal tract. However, the effects of IL-36G during cancer development including gastric cancer remain unexplored. Here, we show that IL-36G induced ERK1/2 activation in AGS, MKN1 and MKN45 human gastric cancer cell lines. Moreover, IL-36G induced colony formation, migration and invasion of these gastric cancer cell lines that was inhibited by the natural antagonist, IL-36 receptor antagonist (RA). Interrogation of TCGA stomach adenocarcinoma patient datasets revealed highly elevated IL-36G gene expression in human gastric cancer compared to normal tissue independent of tumor stage, and high IL-36G expression corresponded with poorer patient survival. Collectively, our results indicate for the first time that IL-36G supports a neoplastic phenotype in human gastric cancer cells.

Colony Formation in Three Species of the Family Scenedesmaceae (Desmodesmus subspicatus, Scenedesmus Acutus, Tetradesmus Dimorphus) Exposed to Sodium Dodecyl Sulfate and its Interference with Grazing of DAPHNIA Galeata.

By mimicking the info-chemicals emitted by grazers, the common anionic surfactant sodium dodecyl sulfate (SDS) can induce colony formation in the green algal genus Scenedesmus at environmentally relevant concentrations. The morphometric effects can hinder the feeding efficiency of grazers, reducing energy flow along the pelagic food chain from Scenedesmus to consumers. Despite this potential ecological risk, few studies exist on whether the SDS-triggered induction of colonies is common in other species of the family Scenedesmaceae. Here, we investigated the effects of SDS on the growth and morphology of three species of Scenedesmaceae (Desmodesmus subspicatus, Scenedesmus acutus, and Tetradesmus dimorphus) and on the clearance rates of Daphnia galeata grazing on the SDS-induced colonies. SDS triggered colony formation in all algal species at concentrations nonlethal to them (0.1-10mg L-1) in 72h; however, the induction levels of colony formation were generally lower than for those in the Daphnia culture medium. We also found that the SDS-induced colonial algae reduced D. galeata clearance rates. Our results highlight the potential effect of SDS on the Daphnia-Scenedesmaceae system by triggering the morphological response of Scenedesmaceae at concentrations below those that exert toxicity. Such disruptive effects of pollutants on predator-prey interactions should be considered within the framework of ecological risk assessments.

Alginate encapsulation induce colony formation with umbilical cord-derived mesenchymal stem cells

Aim: The umbilical cord (UC) is a rich source of mesenchymal stem cell (MSC) isolation. Since the MSCs isolated from here have high self-renewal capacity and differentiation potential, production through biofabrication is essential for clinical treatments. For the cells to be stored for a long time and presented ready for use, encapsulation is required. In this study, UC-MSC cells were encapsulated with alginate using three different methods: alginate drop, alginate coating, and alginate sphere. Methods: The cell viability, live/dead cell ratio, and colony formation capacities of the encapsulated cells were examined for 14 days. Results: In the study, it was found that the most effective method was the alginate sphere form and that the structure of the cells should be preserved by injecting them into biomaterials in encapsulation. Colony formation potential was found to be high in biomaterials with alginate spheres. Conclusion: As a result, the preservation of UC-MSC cells with alginate sphere encapsulation via biofabrication and their clinical use availability may be beneficial for treating of many diseases.

The Effect of pH and Light on the Colony Formation and Buoyancy of Microcystis aeruginosa UTEX-2061

Extracellular polysaccharides (EPS) in the outer layer of Microcystis cells can influence colony formation and buoyancy ability. The carboxyl groups in EPS can combine with divalent metals to induce colony formation. One of the main components in EPS is called tightly cell-bound EPS (TB-EPS), which contains more carboxyl groups and potential to combine with more metal ions. In this study, we isolated the EPS and TB-EPS from Microcystis bloom sample, and, using both EPS samples, the effect of EPS and TB-EPS on the colony formation and buoyancy of M. aeruginosa UTEX-2061 was investigated. Then, we discussed the impact of the environmental factors such as light and solution pH on M. aeruginosa UTEX-2061 colony formation and buoyancy. With the addition of Ca2+, Mg2+, EPS, and TB-EPS, M. aeruginosa UTEX-2061 could form a colony, in which the size was more than 200 μm, showing the same strong buoyancy as wild Microcystis. The addition of TB-EPS could lead to M. aeruginosa UTEX-2061 to form the largest colony and exhibit strong buoyancy under light conditions. Under dark conditions, the addition of EPS or TB-EPS failed to lead M. aeruginosa to form a colony and obtain buoyancy, indicating that light affects colony formation and buoyancy. The solution pH played a role in controlling colony formation and buoyancy. Neutral conditions (pH 7) were conducive for TB-EPS to induce colony formation, while under alkaline conditions (pH 10), EPS had an excellent effect on the induction of M. aeruginosa UTEX-2061 colony formation.

Metabolic Insights Into Infochemicals Induced Colony Formation and Flocculation in Scenedesmus subspicatus Unraveled by Quantitative Proteomics.

Microalgae can respond to natural cues from crustacean grazers, such as Daphnia, by forming colonies and aggregations called flocs. Combining microalgal biology, physiological ecology, and quantitative proteomics, we identified how infochemicals from Daphnia trigger physiological and cellular level changes in the microalga Scenedesmus subspicatus, underpinning colony formation and flocculation. We discovered that flocculation occurs at an energy-demanding ‘alarm’ phase, with an important role proposed in cysteine synthesis. Flocculation appeared to be initially stimulated by the production of an extracellular matrix where polysaccharides and fatty acids were present, and later sustained at an ‘acclimation’ stage through mitogen-activated protein kinase (MAPK) signaling cascades. Colony formation required investment into fatty acid metabolism, likely linked to separation of membranes during cell division. Higher energy demands were required at the alarm phase, which subsequently decreased at the acclimation stage, thus suggesting a trade-off between colony formation and flocculation. From an ecological and evolutionary perspective, our findings represent an improved understanding of the effect of infochemicals on microalgae-grazers interactions, and how they can therefore potentially impact on the structure of aquatic communities. Moreover, the mechanisms revealed are of interest in algal biotechnology, for exploitation in low-cost, sustainable microalgal biomass harvesting.

Nicotine exposure potentiates lung tumorigenesis by perturbing cellular surveillance

BackgroundNicotine is a major tobacco component and found at circulating concentrations in smokers’ bloodstreams. Although considered a non-carcinogenic substance, nicotine rapidly defuses to tissues after being inhaled, inviting effects on cellular physiology, particularly in the lung. Widespread increased use of nicotine-based e-cigarettes, especially in younger adults, creates an urgent need for improved understanding of nicotine’s potential to impact human health.MethodsBiological and biochemistry methods were used to interrogate the potential for nicotine to weaken the genetic integrity of murine and human-lung epithelial cells.ResultsWe demonstrate that nicotine potentiates the growth of the lung epithelial cells in a dose–response fashion. Nicotine elicits an acute increase in reactive oxygen species (ROS), which persists at moderately high levels throughout the duration of nicotine exposure. The aberrant increases in ROS appear to induce ER stress and UPR activation, as reflected by BIP upregulation and PERK phosphorylation. Furthermore, prolonged nicotine exposure interferes with p53 function triggered by sodium arsenite. Unless p53 is suppressed, persistent nicotine exposure does not induce colony formation by lung epithelial cells in soft agar.ConclusionThe data suggest that nicotine treatment, by perturbing intracellular redox state and altering p53 function, can create a pro-tumorigenic environment in lung epithelium. The results suggest caution in using nicotine replacement therapies and e-cigarettes.

Functional Analysis of Trichodysplasia Spinulosa-Associated Polyomavirus-Encoded Large T Antigen.

Trichodysplasia spinulosa-associated polyomavirus (TSPyV or human polyomavirus 8) was identified from patients with trichodysplasia spinulosa, a rare skin disease affecting the faces of immunocompromised patients. Like other polyomaviruses, the TSPyV genome encodes a large T antigen (LT). However, the expression and functions of TSPyV LT in infected cells remain largely unknown. In the present study, we cloned a full-length TSPyV LT cDNA from cells transfected with the full-length of TSPyV LT DNA. Transfection study using green fluorescence protein-tagged LT expression plasmids showed that TSPyV LT was expressed in the nucleus of transfected cells. Analysis of deletion mutants identified a nuclear localization signal in TSPyV LT. Recombinant TSPyV LT exhibited an ATPase activity. TSPyV LT has a chitinase-like domain; however, no chitinase activity was detected. Immunoprecipitation assays revealed that TSPyV LT bound to retinoblastoma 1, but not to p53 in transfected cells. Expression of TSPyV LT in NIH3T3 cells induced colony formation in soft agar, suggesting its transformation activity. These data indicate that TSPyV LT may be associated with the pathogenesis of trichodysplasia spinulosa, which is a hyperplasia of keratinocytes in inner hair follicles.

Extracellular Microenvironmental Change by B16F10 Melanoma-derived Proteins Induces Cancer Stem-like Cell Properties from NIH3T3 Cells

Cancer stem-like cells (CSCs) can generate solid tumors through the properties of stem cells such as self-renewal and differentiation and they cause drug resistance, metastasis and recurrence. Therefore, establishing CSC lines is necessary to conduct various studies such as on the identification of CSC origin and specific targeted therapies. In this study, we stimulated NIH3T3 fibroblasts to exhibit the characteristics of CSCs using the whole protein lysates of B16F10 melanoma cells. As a result, we induced colony formation that displayed self-renewal and differentiation capacities through anchorage-independent culture and re-attached culture. Moreover, colonies showed drug resistance by being maintained in the G0/G1 state. Colonies expressed various CSC markers and displayed high-level drug efflux capacity. Additionally, colonies clearly demonstrated tumorigenic ability by forming a solid tumor in vivo. These results show that proteins of cancer cells could transform normal cells into CSCs by increasing expression of CSC markers. This study argues the tremendous importance of the extracellular microenvironmental effect on the generation of CSCs. It also provides a simple experimental method for deriving CSCs that could be based on the development of targeted therapy techniques.

Control of the buoyancy of Microcystis aeruginosa via colony formation induced by regulating extracellular polysaccharides and cationic ions

It is well recognized that gas vesicles influence the buoyancy of Microcystis and control the migration in the water column. Some of Microcystis strains do not have gas vesicles, so these strains cannot obtain buoyancy from them. In this study, we used two types of Microcystis strains such as the non-gas vesicle synthesizing strain M. aeruginosa UTEX-2061 and the gas vesicle synthesizing strain M. aeruginosa NIES-843 in the buoyancy control experiments of M. aeruginosa. By inducing colony formation and calculating the relative buoyancy rate of each strain, it was proven that the colony formation was strictly related to the buoyancy of both Microcystis strains. M. aeruginosa NIES-843 possessing gas vesicles could obtain buoyancy under the lower concentration of calcium and magnesium than M. aeruginosa UTEX-2061 possessing no gas vesicles. With the addition of the extracellular polysaccharides (EPS) extracted from Microcystis blooms into the culture medium, M. aeruginosa NIES-843 and UTEX-2061 could present higher buoyancy at the lowest concentrations of calcium and magnesium. It was suggested that EPS combined with the divalent metal cations such as calcium and magnesium made Microcystis form colony effectively. Calcium and magnesium ions enhanced the ability of colony formation of Microcystis and had a significant influence on buoyancy.

Chelerythrine induces apoptosis via ROS-mediated endoplasmic reticulum stress and STAT3 pathways in human renal cell carcinoma.

Renal cell carcinoma (RCC) is a heterogeneous histological disease and it is one of the most common kidney cancer. The treatment of RCC has been improved for the past few years, but its mortality still remains high. Chelerythrine (CHE) is a natural benzo[c]phenanthridine alkaloid and a widely used broad‐range protein kinase C inhibitor which has anti‐cancer effect on various types of human cancer cells. However, its effect on RCC has not been fully elucidated. In this study, we evaluated the effect and mechanism of CHE on RCC cells. Our study showed that CHE induced colony formation inhibition and G2/M cell cycle arrest in a dose‐dependent manner in RCC cells. In addition, CHE increased cellular ROS level, leading to endoplasmic reticulum (ER) stress, inactivating STAT3 activities and inducing apoptosis in RCC cells which were suppressed by NAC, a special ROS inhibitor. We further found that both knockdown of ATF4 protein and overexpression of STAT3 protein could reduce CHE‐induced apoptosis in Caki cells. These results demonstrated that the apoptosis induced by CHE was mediated by ROS‐caused ER stress and STAT3 inactivation. Collectively, our studies provided support for CHE as a potential new therapeutic agent for the management of RCC.

EXTL3-interacting endometriosis-specific serum factors induce colony formation of endometrial stromal cells

Endometriosis is a benign chronic condition characterized by the existence of endometrial-like stroma and glandular tissue in extrauterine locations. The molecular mechanisms of its pathogenesis have not been elucidated. We have studied the role of EXTL3 (exostosin-like 3) in endometriosis and found that it is expressed in endometrial tissue as well as endometriosis lesions. We have found that serum from endometriosis patients contains a factor or factors, which interact with EXTL3 resulting in strongly increased colony formation in regenerating cell culture. We also found increased anti-EXTL3 antibodies in endometriosis patients’ sera. EXTL3 is an N-acetyl glucosamine (GlcNAc) transferase, performing a key step in heparan sulfate (HS) glucosaminoglycan synthesis. Many viruses replicate in regenerating epithelial cells and use HS as a receptor for cell entry. We measured antibody titres to viruses, which use HS as a receptor for cell entry, and found rarely increased titres for these viruses in endometriosis sera, whereas titres to viruses using other receptors were equally distributed in study groups. The data indicate that perturbation of HS metabolism is associated with endometriosis.

Allelopathic effects and potential active substances of Ceratophyllum demersum L. on Chlorella vulgaris Beij.

Morphological responses of green algae to submerged macrophytes were rarely studied, and the potential active substances played roles in the interaction were little known previously. In the current work, according to acetone extract experiments, it was demonstrated that submerged macrophytes (Ceratophyllum demersum L.) could allelopathically inhibit the growth of Chlorella vulgaris Beij. and induce its colony formation, the effects of which were concentration dependent. Gas chromatography–mass spectrometry analysis revealed eight kinds of active substances from the C. demersum extracts, namely hexanoic acid, phthalic acid, octanedioic acid, butenoic acid, azelaic acid, palmitic acid, alpha linolenic acid and pentanedioic acid. Standard compound addition test indicated that palmitic acid and alpha linolenic acid might play important roles in the induction of colony formation and growth inhibition of C. vulgaris. This study provided some more new insights into the photosynthetic organism interaction between submerged macrophytes and green algae, in terms of not only growth but also morphological responses.

The potential value of lncRNA-BC050642 in osteosarcoma origination and outcomes

Background The purpose of our research was to explore potential value of lncRNA-BC050642 in osteosarcoma origination and prognosis. Methods In this study, the tissue specimens were collected from 97 osteosarcoma patients and 97 age-matched healthy controls. Besides, human osteosarcoma cell lines U2OS and normal osteoblastic cell line hFOB1.19 were selected for experiments in vitro. lncRNA-BC050642 levels were measured through quantitative real-time polymerase chain reaction (qRT-PCR). Relative expression of the gene c-myc was determined via ELISA analysis. x 2 test was implemented to appraise possible relationship between BC050642 level and clinicopathological features. Cell proliferation assay, plate colony formation assay, and cell apoptosis assay were adopted to analyze the influence of BC050642 on tumor development. Besides, prognostic value of BC050642 was estimated using Kaplan–Meier and cox regression analysis. Results BC050642 levels showed distinctive increases in osteosarcoma tissues and cell lines compared with controls. And c-myc expression was down-regulated in osteosarcoma. There was a negative correlation between the expressions of BC050642 and c-myc. BC050642 expression was proved to be significantly correlated with Ennking and histological type. Up-regulated BC050642 could promote cell proliferation, induce colony formation and meanwhile inhibit cell apoptosis. Conclusions BC050642 is up-regulated in osteosarcma and its over-expression promotes tumor development via down-regulating the expression of c-myc. It also may be an independent prognostic biomarker for osteosarcoma.