MiR-19a promotes epithelial-mesenchymal transition through PI3K/AKT pathway in gastric cancer

AIM: To investigate the mechanism by which mi R-19 a is up-regulated in gastric cancer(GC), which plays an oncogenic role.METHODS: In the present study, we investigated the role of mi R-19 a in gastric tissues as well as two GC cell lines. In vivo, we detected the basal expression level of mi R-19 a using real-time reverse transcription-PCR(RTPCR), and the relevance between expression of mi R-19 a and clinicopathological information was analyzed.In vitro, mi R-19 a was ectopically expressed using overexpression and knock-down strategies.RESULTS: Overexpression of mi R-19 a was significantly associated with metastasis of GC and inferior overall prognosis. However, no significant correlation was f o u n d b e t w e e n m i R- 1 9 a e x p r e s s i o n a n d o t h e r characteristics such as age, gender, tobacco, alcohol or tumor size. Cell proliferation, migration and invasion assays showed that overexpression of mi R-19 a promoted the proliferation, migration and invasion, and that overexpression of mi R-19 a promoted the epithelialmesenchymal transition through activating the PI3K/AKT pathway. Blocking the PI3K/AKT pathway could cancel the effect of mi R-19 a.CONCLUSION: All together, our results suggest that mi R-19 a could be used as a promising therapeutic target in the treatment of GC.

The expression and significance of the multidrug resistance-related proteins P-gp, MRP and LRP in human non-small cell lung cancer tissues

Objective: To explore the expression and significance of the multidrug resistance-related proteins P-glycopro-tein (P-gp), multidrug resistance-related protein (MRP), lung resistance protein (LRP) in human non-small cell lung cancer (NSCLC) tissues and paratumor tissues. Methods: Immunohistochemistry (IHC) was used to examine the expression level of proteins P-gp, MRP and LRP in 43 samples of NSCLC and 15 samples of paratumor tissues. Results: The expression rates of P-gp, MRP and LRP in 43 tumor tissues were 74.42% (32/43), 67.44% (29/43) and 88.37% (38/43), respectively, while in 15 paratumor tissues were 13.33% (2/15), 20.00% (3/15) and 6.67% (1/15), respectively. There was significant difference in the expression of proteins (P-gp, MRP and LRP) between lung cancer tissues and paratumor tissues (P < 0.05). The expres-sion of proteins P-gp, LRP in lung adenocarcinoma were higher than that in other pathological carcinomas (P < 0.05). The expression of protein MRP was not related to pathological type, clinical stage and classification of histodifferentiation (P > 0.05). Conclusion: Multidrug resistance is more common in NSCLC. The proteins of P-gp, MRP and LRP participated in the formation of multidrug resistance in lung cancer. Detection of multidrug resistance-related proteins in lung cancer tissues may be useful to choice drugs.

p53 siRNA promotes autophagy of U2OS cells through its target gene Rap2B

The present study aims to explore the effects of p53 and its target gene Rap2B on the autophagy of U2OS cells.U2OS cells were treated with siRNA against p53,Rap2B,and PLCε.Relative expressions of p53,Rap2B,and PLCεwere determined using quantitative polymerase chain reaction(qPCR)and Western blotting,respectively.Levels of IP3 in the cells were determined using Enzyme-linked Immunosorbent Assay(ELISA).Levels of Ca^(2+) were detected using Flow cytometry.Fluorescence microscopy was used to observe the autophagy of cells.Knockdown of p53 significantly decreased the expressions of Rap2B protein.Additionally,knockdown of p53 significantly decreased the mRNA levels of PLCε.The knockdown of p53,Rap2B,and PLCεsignificantly decreased the levels of intracellular IP3 and Ca^(2+) and promoted autophagy of U2OS cells.Our results demonstrated that p53-Rap2B-PLCε-IP3 signaling pathway regulated autophagy of U2OS cells.