Now that’s using your head: a sea slug’s severed noggin sprouts a new body

Effect of Graphene Film for Surface Modification on Slug Bubble Dynamics in Downward-facing Boiling

1. Bergey E. A., Figueroa L. L., Mather C. M., Martin R. J., Ray E. J., Kurien J. T., Westrop D. R., Suriyawong P. 2014. Trading in snails: plant nurseries as transport hubs for non-native species. Biological Invasions 16: 1441–1451. https://doi.org/10.1007/s10530.... CrossRef Google Scholar

Notch Signaling Pathway Regulates Epithelial-mesenchymal Transition of Osteosarcoma by Activating Slug

Objective To investigate the role and possible mechanism of long non-coding RNA KCNQ1 opposite strand transcript 1 (KCNQ1OT1) in the development of cisplatin (DDP) resistance in osteosarcoma (OS). Methods The expression of KCNQ1OT1 in parental cells and drug-resistant cells was detected by real-time polymerase chain reaction (qPCR). The small interfering RNA (siRNA) targeting lncRNA-KCNQ1OT1 was synthetized and transfected into osteosarcoma cells. The cisplatin sensitivity half maximal inhibitory concentration (IC50), migration and invasion of OS cells were assessed with WST-1 assays and Transwell assays, respectively. The expression of epithelial-mesenchymal transition (EMT) associated molecules was detected by qPCR. Results The IC50 values of cisplatin-resistant MG63/DDP and 143B/DDP in osteosarcoma were (17.960±0.153) μmol/L and (7.725±0.183) μmol/L, respectively, which were significantly higher than the IC50 value of the parental cells [(5.074±0.159), (2.633±0.219) μmol/L] (t=101.148, 30.903, P<0.01). The relative expression levels of KCNQ1OT1 in MG63/DDP and 143B/DDP cells were 6.830±0.105 and 6.284±0.465, respectively, compared with parental cells (3.081±0.167, 2.014±0.216), the difference was statistically significant (t=22.917, 11.722, P<0.01). Knocking down the expression of KCNQ1OT1 can inhibit the migration and invasion of osteosarcoma DDP-resistant cells. After down-regulation of KCNQ1OT1, IC50 values of MG63/DDP and 143B/DDP were decreasedsignificantly. The expression of E-cadherin was down-regulated in the drug-resistant cells, and the expression of N-cadherin and Vimentin was up-regulated. After interference with KCNQ1OT1, the expression of E-cadherin was up-regulated and the expression of N-cadherin, Vimentin and Slug was down-regulated. Conclusion KCNQ1OT1 may promote osteosarcoma cisplatin resistance by regulating EMT. KCNQ1OT1 may be a potential therapeutic target for DDP-resistant osteosarcoma Key words: Long non-coding RNA; KCNQ1 opposite strand transcript 1; Osteosarcoma

The aluminium industry is one of the largest emitters of greenhouse gases (GHG) and accounts for approximately 1 % of global GHG emissions. A large portion of emissions are indirect emissions, due to the large GHG footprint of consumed electricity, while direct energy and process-related emissions are also significant. The aluminium is widely used in packaging, transportation, the building sector and for various other purposes. This study focuses on aluminium slugs, which are semi products made from aluminium alloys and are used as tubes and containers in the pharmaceutical, food and cosmetic industries. Since the aluminium industry is among the largest GHG emitters, a Life Cycle Assessment (LCA) was performed to evaluate the environmental impact of aluminium slug production. Environmental impact assessment was performed using OpenLCA software, the Ecoinvent 3.1 database and self-collected plant data. The study includes the environmental impact of anode production, electrolysis and slug production. The functional unit for the study is 1 t of aluminium slug at the company exit gate. Besides GHG emissions and the related GHG footprint associated with slug production, acidification potential and photochemical oxidation potential are further assessed. Various opportunities for GHG emission reduction are further investigated in accordance with the longer-term company strategy. If more aluminium scrap were used and carbon capture performed, the GHG footprint could be reduced by 65 % compared to the base case.

Objective To study the effect of low expression of tumor necrosis factor receptor associated factor 4 (TRAF4) on invasion and migration of colorectal cancer cells. Methods Immunohistochemistry was used to detect the expression of TRAF4 in clinical specimens of colorectal cancer and the adjacent tissues. The expression levels of epithelial-mesenchymal transition (EMT)-related proteins [E-cadherin (E-cad), Snail and Slug] were detected by Western blotting. The Transwell assay was used to examine the invasive ability and migration ability of tumor cells LoVo after silencing TRAF4. Results Immunohistochemistry showed that TRAF4 expression was significantly higher in cancer tissues than in adjacent tissues (t=8.322, P<0.01). After transfection with TRAF4 small interfering RNA (siRNA), the expression of TRAF4 was significantly decreased (t=7.687, P<0.01), the expression of E-cad was increased (t=4.322, P<0.05), the expression of Snail and Slug was decreased (t=9.831, P<0.01, t=8.677, P<0.01), and the invasion and migration ability was obviously decreased (t=9.553, P<0.01, t=11.290, P<0.01). Conclusion Silencing TRAF4 can inhibit the invasion and migration of colorectal cancer cell LoVo. Key words: Colorectal cancer; Tumor necrosis factor receptor associated factor 4; Invasion; Migration; Epithelial-mesenchymal transition

Objective To evaluate the role of circular RNA protein arginine methyltransferase 5 (circPRMT5) in the genesis and progression of colorectal cancer. Methods From January 2013 to December 2017, 96 patients with colorectal cancer who underwent radical resection in Department of General Surgery, Jiading District Central Hospital Affiliated to Shanghai Medical College of Health were collected. The expression of circPRMT5 in colorectal cancer tissues was examined by real-time polymerase chain reaction (RT-PCR). The correlation between circPRMT5 expression level and age, gender, tumor size, tumor location, pathological differentiation, TNM stage, lymph node metastasis of patients with colorectal cancer was analyzed. The SW620 and LOVO cells were divided into control group, circPRMT5-lenti group and circPRMT5-shRNA-lenti group according to different interventions. The effects of circPRMT5 expression level on viability, apoptosis, mitochondrial membrane potential and migration of SW620 and LOVO cells were detected. The influence of circPRMT5 expression level on E-cadherin, Slug, N-cadherin and vimentin was determined by Western blotting method. The potential target miRNA of circPRMT5 was predicted by Starbase V2.0. Student′s t test, analysis of variance and chi-square test were performed for statistical analysis. Results The results of RT-PCR showed that the expression of circPRMT5 in colorectal cancer tissues was higher than that of adjacent cancer tissues (2.167±0.345 vs. 1.103±0.144), and the difference was statistically significant (t=26.847, P<0.01). The circPRMT5 expression level was positively correlated with tumor size, TNM stage, lymph node metastasis and distant metastasis (χ2=6.010, 10.971, 5.321 and 6.272, all P<0.05). The upregulation of circPRMT5 expression could promote proliferation and migration of SW620 and LOVO cells. The circPRMT5 downregulation could inhibit cell proliferation, induce apoptosis and decrease mitochondrial membrane potential. The results of Western blotting indicated that, compared with those of control group, the expression of Slug, N-cadherin and vimentin increased in circPRMT5-lenti group (1.023±0.038 vs. 2.105±0.042, 1.051±0.309 vs. 2.277±0.111, 1.055±0.040 vs. 2.002±0.537, respectively), however the expression of E-cadherin decreased (2.074±0.214 vs. 0.627±0.023), and the differences were statistically significant (t=31.817, 22.065, 14.536 and 9.148, all P<0.01). Compared with the control group, the expression of Slug, N-cadherin and vimentin decreased in circPRMT5-shRNA-lenti group (1.023±0.038 vs. 0.585±0.023, 1.051±0.309 vs. 0.616±0.043, 1.055±0.040 vs. 0.537±0.022), while the expression of E-cadherin increased (2.074±0.214 vs. 2.756±0.148), and the differences were statistically significant (t=-13.795, -14.252, -11.794 and -13.116, all P<0.05). A total of 21 miRNAs might have potential binding sites with circPRMT5 predicted by Starbase V2.0 software. The expression of miRNA4735-3p, miRNA202-3p, miRNA326, let-7i-5p and miRNA4500 was negatively correlated with circPRMT5 expression in both SW620 and LOVO cells confirmed by RT-PCR. Conclusion CircPRMT5 is an important oncogenic gene in the genesis and progress of colorectal cancer, and may have certain potential application prospect in the research and development for colorectal cancer. Key words: Colorectal neoplasms; circPRMT5; Epithelial-mesenchymal transition

Slugs are serious pests of horticulture and agricultural crops. Beside the ability of some plant growth regulators to regulate the growth of cultivated plants, they have Eco-toxicological effects on some invertebrates. So the present study was performed to evaluate the biological toxicity of sublethal concentrations (200 and 400 µl/l) of the plant growth regulator (PGR), Esrel (48% Ethephon), on Deroceras reticulatum after 2 weeks of exposure. The LC50 and LC90 were 980 and1500 µl/l, respectively. The obtained results indicated that PGR treatment led to a significant decrease in growth rate (P≤0.05), by the end of experiment it was 1.5 ± 0.03 g, 1.3 ± 0.04 g at the concentrations 200, and 400 µl/l, respectively compared to control (2 ± 0.03 g). In addition, flow cytometric analysis of cell cycle and immunohistochemical assays recorded DNA damage in digestive gland cells of D. reticulatum. The percentage of apoptosis was 78% and 93% at the concentration 200 and 400 µl/l, respectively, compared with control (8%). The study concluded that Esrel has toxic and apoptotic effects on D. reticulatum, so it has been proposed that the Esrel can be used as a molluscicide for the slug, Deroceras reticulatum.

Objective To ascertain the specific activities of nigericin on inhibiting human epithelial ovarian cancer (EOC) cells, and to investigate the possible molecular mechanism of nigericin on cell migration and invasion. Methods Cell viability under different treatments of nigericin (0.312 5, 0.625, 1.25, 2.5, 5, 10, 20, 40, 80 μmol/L) on EOC A2780 and SKOV3 cell lines was examined by CCK-8 assay, with DMSO as a control. The human epithelial ovarian cancer cell lines A2780 and SKOV3 were treated with 5, 10 or 20 μmol/L nigericin or with DMSO as a control. Transwell chambers was used to observe the impact of nigericin on migration and invasion of EOC cells. Western blot was used to detect the expressions of epithelial cell marker (E-cadherin), mesenchymal cell marker (Vimentin) and the epithelial-mesenchymal transition (EMT)-related transcription factors Slug, Snail, and Twist, as well as the expressions of proteins related to Wnt/β-catenin signaling pathway such as Gsk-3β, p-Gsk-3β and β-catenin under different concentration treatment of nigericin. Results CCK-8 assay showed that nigericin exhibited strong cytotoxicity on A2780 [IC50 (16.19±0.26) μmol/L, 95% CI 1.077-1.341)] and SKOV3 [IC50 (11.87±0.21) μmol/L, 95% CI 1.003-1.146] cell lines. Transwell chamber assay revealed that nigericin at different concentration (5, 10, 20 μmol/L) induced a remarkable reduction in the number of cells migrating through the membrane relative to the vehicle-treated controls in A2780 and SKOV3 cells [(121±9), (92±7), (59±5)/HP and (120.4±2.6), (91.8±5.5), (80.0±4.0)/HP, all P < 0.05]; the invasive ability of A2780 and SKOV3 cells also inhibited [(61.2±3.7), (43.2±4.3), (23.6±2.1)/HP and (85.2±7.0), (65.2±4.6), (45.6±4.4)/HP, all P < 0.05]. Western blot revealed that the increased expression of E-cadherin and decreased expression of Vimentin, Slug, Snail, Twist, p-Gsk-3β, β-catenin in EOC cells with the nigericin treatment at different concentration (5, 10 and 20 μmol/L) showed concentration dependence (P < 0.05). Conclusion Nigericin may induce EMT by activating Wnt-β-catenin signaling pathway to promote the migration and invasion of EOC cells. Key words: Ovarian neoplasms; Nigericin; Epithelial-mesenchymal transition; Migration; Invasion

This is an experimental case study with the objective of evaluating the cicatricial progression of varicose ulcer treated with the gel in natura of Aloe barbadensis Miller in the period of 83 days. The research included a carrier of varicose ulcer with lesions 2nd and 4th toes D, which was not performing topical drug treatment. The dressing was performed daily following the cleaning protocol with gentle irrigation with 0.9% Sodium Chloride heated and covering with the fresh slug gel extracted from the plant bulb just before the dressing time, maintaining a semi- occlusive with sterile and compressive gauze with bandage. The characteristics of the wound and the evolution of the cicatricial process through the photographic imaging, measurement of the lesion bed with the IMAGE J® and registry of the characteristics of the bed of the lesion, borders and peri ulcer region at 29o, 48o, 66o and 83 days of treatment. The results indicate that the use of phytotherapics promoted the control of inflammatory signs, improved hydration and vascularization of the lesions and peri ulcer regions and cellular regeneration, promoting at the end of the treatment total healing of the ulcer present in the 4th right foot podactylus and important reduction of the area of the other injuries. However, in order to produce evidence for the practice it is necessary to develop other experimental studies with an expanded sample to clarify the benefits and mechanisms of action of the herbal medicine in the treatment of varicose ulcers.

Objective To investigate the effects of small interfering RNA (siRNA) CXCR4 gene on proliferation, invasion and epithelial-mesenchymal transition factors including Twist, Slug and E-cadherin (E-cad) in HeLa cells of human cervical carcinoma. Methods HeLa cells were cultured in vitro and CXCR4-siRNA was transfected into HeLa cells. Methyl thiazolyl tetrazolium (MTT) assay was used to detect the changes of cell proliferation. Transwell experiment was used to observe the changes of cell invasion, and the expressions of CXCR4, Twist, Slug and E-cad protein were detected by Western blot. Results Compared with the blank control group and the negative control group, CXCR4-siRNA transfected into HeLa cells significantly inhibited the expression of CXCR4 protein (0.959±0.197, 0.932±0.141 vs. 0.379±0.022 respectively; F=16.286, P=0.004). MTT results showed that the proliferation of HeLa cells was inhibited at 48 h and 72 h (48 h: 0.846 ± 0.034, 0.823 ± 0.025 vs. 0.744 ± 0.039, F= 7.379, P= 0.024; 72 h: 0.996±0.026, 0.964±0.059 vs. 0.829±0.051, F= 10.425, P= 0.011). Transwell results showed that the invasiveness of HeLa cells in CXCR4-siRNA group was inhibited at 48 h and 72 h (cell membrane number, 48 h: 37.4±8.1, 33.6±6.2 vs. 25.4±3.2, F = 4.830, P = 0.029. 72 h: 48.4±7.6, 43.0±5.4 vs. 33.4±6.7, F = 6.579, P = 0.012). After transfection for 48 h, the expression of Twist and Slug protein was decreased and E-cad protein was increased in CXCR4-siRNA group (Twist: 0.93±0.11, 1.00±0.17 vs. 0.53±0.07, F = 10.962, P = 0.010; Slug: 0.515±0.084, 0.470±0.055 vs. 0.190±0.028, F = 25.579, P = 0.001; E-cad: 0.53±0.04, 0.55±0.24 vs. 1.11±0.14, F = 12.494, P = 0.007). Conclusions Silencing CXCR4 gene can inhibit the proliferation and reduce the invasiveness of HeLa cells. Inhibiting EMT of HeLa cells can be achieved by down-regulating the expressions of Twist and Slug protein, and up-regulating the expression of E-cad. Key words: Uterine cervical neoplasms; CXCR4; Epithelial-mesenchymal transition

To investigate the molecular mechanism by which LKB1 regulates epithelial-mesenchymal transition (EMT) in Peutz-Jeghers hamartoma and intestinal epithelial cells. Immunohistochemistry was used to detect gene expression of LKB1, E-cadherin, and vimentin in 20 hamartoma tissues and 10 normal intestinal tissues, and collagen fiber deposition was analyzed using Masson trichrome staining. Normal intestinal epithelial NCM460 cells were transfected with LKB1 shRNA plasmid or negative control via lentiviral vectors, and the role of LKB1 in cell polarization and migration were determined using CCK8 and Transwell assays. Western blotting, quantitative real-time PCR (qPCR) and immunofluorescence were used to assess the alterations of EMT markers in the cells with LKB1 knockdown. Compared with normal intestinal tissues, hamartoma polyps showed significantly decreased LKB1 and E-cadherin expressions and increased vimentin expression with increased collagen fiber deposition. The cells with LKB1 knockdown exhibited enhanced cell proliferation and migration activities (P<0.01). Western blot analysis, qPCR and immunofluorescence all detected decreased E-cadherin and increased N-cadherin, vimentin, Snail, and Slug expressions in the cells with LKB1 knockdown. s LKB1 deficiency triggers EMT in intestinal epithelial cells and Peutz-Jeghers hamartoma, suggesting that EMT can serve as the therapeutic target for treatment of Peutz-Jeghers syndrome.

Objective This study aimed at observing expression and clinical significance of metadherin in gastric adenocarcinoma and exploring the potentially regulating mechanism of metadherin in invation and migration of gastric cancer. Methods Expressions of metadherin and E-cadherin in primary lesion of gastric cancer were detected by immunohistochemistry and their correlation to clinicopathologic characteristics and prognosis were analyzed by Chi-square tests. Transwell assay and wound healing assay were applied for the ability of invasion and metastasis in gastric cancer cells. Then, the down-regulatied metadherin expression in MKN45 cells by RNA interference (siRNA) was carried out and furthermore, the regulation role of metadherin in epithelial-mesenchymal transition was analyzed also in invasion and migration of gastric cancer cells. Results The positive expression of metadherin was correlated to invading depth (P=0.029), lymph node metastasis (P=0.001), TNM stage (P=0.014) and inhibiting E-cadherin expression (P=0.001). The patients with positive metabherin shared poorer prognosis. Furthermore, the down-regulated metabherin in MKN45 cells would result in the increasing expression of E-cadherin, as well as decreasing expression of N-cadherin, Slug and Snail. At the same time, the abilities of invasion (P=0.027) and migration (P=0.008) of MKN45 cells was decreased. Conclusion metabherin induces EMT in metastasis of gastric adenocarcinoma via activating either Slug or Snail but not twist, which would result in the poorer prognosis. Key words: MTDH; Stomach neoplasms; Epithelial-mesenchymal transition; Metastasis; Prognosis; Chi-Square distribution

Objective To observe the expressions of Slug, BRAF V600E and STIP1 proteins in papillary thyroid carcinoma (PTC), and to explore their correlation with capsular invasion and regional lymph node metastasis. Methods Slug, BRAF V600E and STIP1 expressions in 107 cases of differentiated PTC were examined by immunohistochemical staining. The expressions of three proteins and clinicopathological data were statistically analyzed. Results Positive rates of Slug, BRAF V600E and STIP1 in PTC were 65.4% (70/107), 61.7% (66/107) and 66.4% (71/107), respectively, and overexpression of Slug, BRAF V600E and STIP1 was significantly associated with capsular invasion and regional lymph node metastasis in PTC (P < 0.05). There are a significant correlation between expression of Slug and BRAF V600E in PTC (r= 0.235, P < 0.05). Conclusion Overexpression of Slug, BRAF V600E and STIP1 proteins is associated with capsular invasion and regional lymph node metastasis in PTC, which maybe useful for predicting regional lymph node metastasis and prognostic evaluation. Key words: Thyroid neoplasms; Carcinoma, papillary; Slug; BRAF V600E; STIP1; Lymph nodes metastasis; Prognosis

Background: Our previous study has shown that down-regulation of axon guidance repulsive Semaphorin-3F (SEMA3F) promotes growth and metastasis of colorectal cancer (CRC) cells. However, the role of SEMA3F in chemosensitivity and epithelial-mesenchymal transition of CRC cells remains unknown. Methods: The expression of SEMA3F, P-gp, GST-π and TOPO-II in CRC tissues from 94 patients was determined by immunohistochemical staining. Knock-down of SEMA3F was achieved by lentivirus transfection. Functional assays were done to evaluate the invasion, apoptosis and cell viability. Results: We found that the expression of SEMA3F is negatively correlated with the expression of P-gp and GST-π in CRC tissues from 94 patients. Knock-down of SEMA3F significantly decreased apoptosis of HCT116 and SW480 cells, accompanying with up-regulation of anti-apoptotic BCL-2 and down-regulation of pro-apoptotic BAD and BAX. In addition, knock-down of SEMA3F attenuated chemosensitivity to oxaliplatin of CRC cells. Moreover, we found that down-regulation of SEMA3F promotes epithelial-mesenchymal transition of HCT116 and SW480 cells by decreasing the expression of epithelial marker E-cadherin, and increasing the expression of mesenchymal marker Slug, Snail and Vimentin. Finally, knock-down of SEMA3F increased the tumor volume and decreased overall survival of nude mice using colorectal cancer orthotopic xenograft model under the treatment of oxaliplatin. Conclusions: SEMA3F increases chemosensitivity to oxaliplatin and inhibits epithelial-mesenchymal transition of CRC cells.

Earliest mollusk probably looked like a spiky slug

Super Slug of Doom by Matty Long

Liquid Repellantcoatings Inspired by the Secretion Function of Slug's Skin

Recent studies showed that mesenchymal stem cells derived from adipose tissue can promote tumour progression, raising some concerns regarding their use in regenerative medicine. In this context, we co-cultured either SAOS2 osteosarcoma or MCF7 breast cancer cells with human adipose stem cells (hASCs), in order to evaluate potential effects of cancer cells on hASCs differentiation, in vitro and in vivo. In this study we observed that both SAOS2 and MCF7 cell lines induced an increase in hASCs proliferation, compared to hASCs alone, but, surprisingly, neither changes in the expression of CD90, CD29, CD324 and vimentin, nor variations in the Twist and Slug mRNAs were detectable. Noteworthy, SAOS2 and MCF7 cells induced in hASCs an upregulation of CD34 expression and Stemness genes, including OCT3/4, Nanog, Sox2 and leptin, and a decrease in angiogenic factors, including CD31, PDGFα, PDGFRα, PDGFRβ and VEGF. SMAD and pSMAD2/3 increased only in hASCs alone. After 21 days of co-culture, hASCs differentiated both in adipocytes and endothelial cells. Moreover, co-injection of MCF7 cells with hASCs led to the formation of a highly vascularized tumour. Taken together our findings suggest that mesenchymal stem cells, under tumour cell induction, do not differentiate in vitro or facilitate the angiogenesis of the tumour in vivo, thus opening interesting new scenarios in the relationship between cancer and stem cells. These findings may also lead to greater caution, when managing autologous fat grafts in cancer patients.