LINC00355 inhibits apoptosis and promotes proliferation of gastric cancer cells by regulating Wnt/ß-catenin signaling pathway.

OBJECTIVE: To study the expression and biological functions of long intergenic non-protein coding ribonucleic acid 00355 (LINC00355) in gastric cancer (GC), and to explore its potential mechanism of action. PATIENTS AND METHODS: The relative expression level of LINC00355 in 48 cases of GC tissues, the corresponding paracancerous tissues, and GC cells was determined using quantitative reverse transcription-polymerase chain reaction (qRT-PCR), and the interference efficiency of small interfering (si)-LINC00355 was detected via qRT-PCR. After knock-down of LINC00355, methyl thiazolyl tetrazolium (MTT) and 5-ethynyl-2'-deoxyuridine (EdU) assays were performed to detect the changes in the proliferation ability of GC cells, and the changes in the GC cell cycle distribution and apoptosis rate were examined by flow cytometry. Besides, Western blotting was conducted to verify the changes in the downstream signaling pathway of LINC00355. RESULTS: Among 48 cases of GC tissues, there were 42 (87.5%) cases of LINC00355 expression up-regulation, and 6 (12.5%) cases of LINC00355 expression down-regulation. The qRT-PCR results revealed that the expression of LINC00355 was raised in 4 kinds of GC cells. After interference with LINC00355 expression, the MTT assay results indicated that the cell proliferation ability was inhibited, consistent with the EdU assay results. After LINC00355 was knocked down in GC cells, GC cells in experiment group had a higher apoptosis rate than those in si-NC group and arrested in the gap 0 (G0)/G1 phase. Moreover, it was found through Western blotting that the expressions of the molecular markers in the downstream wingless-INT (Wnt)/ß-catenin signaling pathway were downregulated after interference with the expression of LINC00355. CONCLUSIONS: LINC0035 exhibits an up-regulated expression in GC and regulates the Wnt/ß-catenin signaling pathway to promote proliferation and inhibit apoptosis.

MiR-769-5p functions as an oncogene by down-regulating RYBP expression in gastric cancer.

OBJECTIVE: The purpose of this study was to detect the relative expression level of micro-ribonucleic acid (miR)-769-5p in gastric cancer (GC) tissues and cells, and to investigate the clinical significance, biological function, and mechanism of miR-769-5p in GC. PATIENTS AND METHODS: The relative expression level in 62 cases of GC tissues and paracancerous tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The correlation between miR-769-5p expression and clinicopathological characteristics of GC patients was analyzed by Chi-square test. Besides, the relative expression level of miR-769-5p in GC cells and the interference efficiency of si-miR-769-5p were detected by qRT-PCR, and the biological function of miR-769-5p was studied by in vitro experiments [Thiazolyl Blue Tetrazolium Bromide (MTT), flow cytometry, 5-ethynyl-2'-deoxyuridine (EdU)]. Next, the effect of miR-769-5p on the tumorigenicity of GC cells in vivo was investigated by nude mouse tumorigenicity assay. Moreover, the downstream target genes of miR-769-5p were predicted by bioinformatics. Finally, qRT-PCR and Western blotting were used to screen the downstream target genes. RESULTS: In the 62 cases of GC tissues, the expression of miR-769-5p was upregulated in 48 cases. MiR-769-5p was divided into high-expression group and low-expression group. Chi-square analysis showed that the high expression of miR-769-5p was positively correlated with tumor-node-metastasis (TNM) stage (p=0.005), lymph node metastasis (p=0.010), and infiltration depth (p=0.011) in patients with GC. The results of qRT-PCR indicated that the expression of miR-769-5p was upregulated in GC cells. In vitro experiments (MTT, flow cytometry, EdU) results showed that after interfering in the expression of miR-769-5p, the proliferation ability of GC cells was decreased, and apoptosis was increased. Furthermore, the results of in vivo experiments manifested that the tumorigenic ability of GC cells declined after interference in the expression of miR-769-5p. Finally, the results of qRT-PCR and Western blotting revealed that the expression of RING1 and YY1-binding protein (RYBP) was regulated by miR-769-5p. CONCLUSIONS: The expression of miR-769-5p is upregulated in GC and positively correlated with TNM stage in GC patients. By regulating the expression of RYBP, the proliferation of GC cells was promoted, and the apoptosis was inhibited.