Aim: To explore the role of RPL38 on proliferation and apoptosis of gastric cancer cells by regulating miR-374b-5p/VEGF signal pathway. Methods: qRT-PCR was used to measure the expression of RPL38. CCK8 assay, Matrigel invasion assay, and flow cytometry were used to detect the role of RPL38in MKN-45 cells. Western blot was used to measure the protein expression of VEGF, pERK , ERK, p-AKT, AKT in cells. Dual-luciferase assay was performed to verify the relationship between miR-374b-5p and RPL38, miR-374b-5p and VEGF. Results: In our research, we found that RPL38 was upregulation in gastric cancer, loss function of RPL38 could inhibit MKN-45 cell proliferation and invasion, accompany with increasing apoptosis. Then, we verified that RPL38 could interact with miR-374b-5p by performed luciferase assay, there was a negative correlation between RPL38 and miR-374b-5p. Furthermore, we observed that VEGF is a potential target of miR-374b-5p, miR-374b-5p negatively regulated the expression of VEGF, and effected ERK/AKT signal pathways. Next, we found that miR-374b-5p inhibitor or overexpression of VEGF could prevent the antitumor function of si-RPL38. Conclusion: Knockdown of RPL38 inhibits the proliferation and apoptosis of gastric cancer via miR-374b-5p/VEGF signal pathway.

Purpose: lncRNA NEAT1 has been reported as a tumor-promoting gene in a variety of tumors, but few studies have explored its role and mechanism in gastric cancer. In the face of increasing incidence of gastric cancer, how to improve the diagnostic accuracy and therapeutic effect of gastric cancer is a major clinical problem. Therefore, we studied the effect and mechanism of lncRNA NEAT1 on the proliferation, invasion and epithelial-mesenchymal transition of gastric cancer cells. To inquiry into the effect of lncRNA NEAT1 on the proliferation, invasion and epithelial-mesenchymal transition (EMT) of gastric cancer (GC) cells by regulating miR-129-5p/PBX3 axis. Methods: Totally 63 GC diagnosed and treated in our hospital were selected as the study subjects, whose paired GC tissues and pericarcinomatous tissues were collected as the study specimens after obtaining their consent. QRT-PCR was employed to detect the NEAT1 expression in tissues and cells to analyze the relationship between NEAT1 and clinicopathological data of GC patients. In addition, stable and transient overexpression and inhibition vectors were established and transfected into GC cells HCG-27 and MKN-45. CCK-8, traswell, and flow cytometry were employed to evaluate the proliferation, invasion, and apoptosis of transfected cells. The correlation of miR-129-5p between PBX3 and NEAT1 was assessed using dual luciferase reporter assay, while that between NEAT1 and miR-129-5p was assessed by RNA-binding protein immunoprecipitation (RIP) . Western blot was applied for the detection of apoptosis and EMT related proteins.Results: NEAT1 was overexpressed in GC patients and had a high diagnostic value. The expression of NEAT1 was related to the pathological stage, differentiation degree, tumor size and lymph node metastasis of patients with GC. Down-regulated NEAT1 brought decreased cell proliferation, invasion and EMT, and increased apoptosis. According to dual luciferase reporter assay, NEAT1 could target miR-129-5p, while in turn miR-129-5p could target PBX3. Functional analysis exhibited that miR-129-5p overexpression inhibited PBX3 in GC cells, affecting cell proliferation, invasion, EMT and apoptosis, and rescue experiments demonstrated that these effects were eliminated by up-regulating NEAT1 expression.Conclusion: Inhibition of NEAT1 could mediate miR-129-5p/PBX3 axis to promote apoptosis of GC cells, and reduce cell proliferation, invasion and EMT.

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