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Besides, over-expression of lncRNA BCAR4 could activate the MAPK/ERK signaling pathways. Tumor xenograft formation assay demonstrated that over-expression of lncRNA BCAR4 promoted tumor formation in vivo. CONCLUSIONS LncRNA BCAR4 was proved significantly up-regulated in GC. Over-expression of lncRNA BCAR4 promoted cell proliferation and suppressed cell apoptosis in vitro and promoted tumor formation in vivo. Besides, Western blotting revealed that lncRNA BCAR4 played an oncogenic role in GC via regulating MAPK/ERK signaling.OBJECTIVE The aim of this study was to investigate the expression characteristics of LINC01857 in gastric cancer (GCa), and to further study whether it could promote GCa development by modulating microRNA-200b. PATIENTS AND METHODS Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to examine LINC01857 expression in 60 pairs of GCa tissues and adjacent tissues. The interplay between LINC01857 level and clinical indexes and the prognosis of GCa patients was analyzed. Meanwhile, qRT-PCR was used to verify the expression level of LINC01857 in GCa cell lines. LINC01857 knockdown model was constructed by lentivirus transfection in GCa cell lines. Subsequently, the effect of LINC01857 on the biological function of GCa cells was analyzed by Cell Counting Kit 8 (CCK8), wound healing, and transwell assays. Furthermore, the in-depth relationship between LINC01857 and microRNA-200b was explored. RESULTS QRT-PCR results showed that LINC01857 level in GCa tissues was remarkably higher than that of adjacent tissues, and the difference was statistically significant (p less then 0.05). Compared with patients with a low level of LINC01857, the rate of lymph node and distant metastasis in patients with a high level of LINC01857 was remarkably higher, while the overall survival rate was lower (p less then 0.05). In vitro experiments showed that LINC01857 knockdown remarkably decreased the invasion, migration, and crawling ability of GCa cells (p less then 0.05). Subsequent qRT-PCR results demonstrated that the level of microRNA-200b was remarkably upregulated after the silence of LINC01857. In addition, the silence of microRNA-200b could reverse the biological function of GCa cells induced by the knockout of LINC01857. CONCLUSIONS LINC01857 was highly expressed in GCa, and was associated with lymph node metastasis, distant metastasis, and poor prognosis of patients with GCa. In addition, LINC01857 enhanced the metastatic ability of GCa cells by regulating microRNA-200b.OBJECTIVE To clarify the role of HMGA1 in influencing proliferation and migration abilities, and EMT (epithelial-mesenchymal transition) in gastric cancer (GC) cells. MATERIALS AND METHODS Differential expressions of HMGA1 in GC tissues and normal gastric tissues were analyzed in the GEPIA dataset. Its influence on overall survival of GC patients was evaluated as well. Moreover, HMGA1 levels in GC cells and gastric mucosal cells were detected. Regulatory effects of HMGA1 on the proliferation and migration abilities in SGC7901 and MGC803 cells were assessed through a series of functional experiments. At last, influences of HMGA1 on the expression levels of EMT-related genes, E-cadherin, Snail, and Slug were determined in GC cells. RESULTS Analysis of data in TCGA GEPIA dataset revealed that HMGA1 was upregulated in GC tissues, and GC patients with a high expression level of HMGA1 suffered poorer prognosis. In addition, HMGA1 was identically upregulated in GC cells, and the overexpression of HMGA1 improved the proliferation and migration abilities of SGC7901 and MGC803 cells, downregulated E-cadherin, and upregulated Snail and Slug in GC cells, while silence of HMAG1 yielded the opposite results CONCLUSIONS HMGA1 is upregulated in GC tissues and predicts poor prognosis, and it aggravates the progression of GC via stimulating EMT.OBJECTIVE This meta-analysis aims to clarify the effect of IL-17 polymorphisms on the susceptibility to GCa in the Chinese population. MATERIALS AND METHODS Relevant pieces of literature were searched in PubMed, Web of School, VIP, and CNKI using the key words as “IL-17, gastric/stomach cancer” or “IL-17 polymorphisms, gastric/stomach cancer susceptibility”. The odds ratio (OR) and 95% confidence interval (CI) in the selected studies were calculated using RevMan5.3 and STATA12.0. RESULTS A total of 12 investigations reporting mutations in IL-17A rs2275913 and IL-17F rs763780 were enrolled. There were 11 studies reporting rs2275913 G>A, involving 3299 cases of GCa patients and 3339 cases of healthy controls. The random-effects model was performed since the heterogeneity test results of the recessive genetic model (GG&GA vs. AA) and the allelic model (G vs. A) of IL-17A rs2275913 G>A were I2>66%/p=0.001. Meanwhile, the dominant genetic model (GG vs. GA&AA) and the super-dominant genetic model (GA vs. GG&AA) of IL-17A rs2275913 G>A were I2C polymorphism is positively correlated with GCa susceptibility in the super-dominant model.OBJECTIVE To elucidate the expression and influence of Linc00702 on the development and progression of colorectal cancer (CRC). selleck kinase inhibitor PATIENTS AND METHODS The expression of Linc00702 was evaluated using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) in 91 paired CRC tissue samples and adjacent normal tissue samples, as well as in CRC cell lines. Cell proliferation in Caco2 and SW620 cells was detected using colony formation assay and 5-Ethynyl-2′-deoxyuridine (EdU) assay. Wound-healing assay and transwell analysis were utilized to assess the abilities of cell migration and invasion. Western blot analysis was employed to further explore the underlying mechanism of Linc00702 in CRC. RESULTS Linc00702 was lowly expressed in CRC tissues and cells. Over-expression of Linc00702 reduced cell proliferation, migration, and invasion of Caco2 cells, while knockdown of Linc00702 promoted cell growth and metastasis of SW620 cells comparing to control group, relatively. PTEN was verified as the target for Linc00702 in CRC, and Linc00702 promoted PTEN expression to inhibit the PI3K/AKT pathway. CONCLUSIONS Linc00702 was downregulated in CRC and inhibited cell proliferation, migration, and invasion by repressing the PI3K/AKT pathway via promoting PTEN expression. This might provide a new target for the biological treatment for CRC.