To investigate the role of long chain non-coding RNA00707 (lncRNA00707) and micro RNA-613 (miR-613) in regulating the proliferation and metastasis of gastric cancer cells and its underlying mechanisms. Methods: Eighty-nine pairs of primary gastric cancer tissues and corresponding prar-cancerous tissues were collected from the Department of Surgical Oncology, Qinghai Provincial People's Hospital during January 2014 and June 2018 for this study. The expressions of lncRNA00707 and miR-613 in gastric cancer tissues and cells were detected by qPCR. The lncRNA00707 low expression and over-expression models of MGC-803 and SGC-7901 cells were established; The proliferation of gastric cancer cells was monitored by CCK-8 assay, and Transwell assay was performed to determine the migration and invasion of gastric cancer cells. Dual luciferase gene reporter assay was adopted to validate the relationship between lncRNA 00707 and miR-613. Results: Compared with para-cancerous tissues and normal cell line GES-1, the expression of lncRNA 00707 was significantly up-regulated in cancer tissues and cell lines, and the expression of lncRNA00707 was positively correlated with WHO stage (all P<0.05). Down-regulation of lncRNA 00707 significantly inhibited the proliferation and migration of SGC-7901 cells, while overexpression of lncRNA00707 exerted the opposite effect (all P<0.05). Compared with negative control group, lncRNA00707 over-expression significantly reduced the luciferase activity of miR-613; in the contrary, the luciferase activity of miR-163 was significantly increased in MGC-803 and SGC-7901 cells with lncRNA 00707 knockdown (all P<0.01). Conclusion: lncRNA 00707 facilitates the proliferation, migration and invasion of gastric cancer cells by inhibiting the function of miR-613, which exerts a protumorigenic effect in gastric cancer.

Objective : To study the mechanism of neurotrophin receptor⁃interacting MAGE homolog (NRAGE) on the proliferation and invasion of colorectal cancer (CRC) cells. Methods : The clinicopathological data of 84 CRC patients were selected. Fluorescence quantitative PCR (qPCR) and Western blot were used to detect the expression of NRAGE in CRC tissues and adjacent normal tissues. The relationship between the expression of NRAGE in cancer tissues and clinicopathological characteristics was analyzed statistically. RT⁃PCR and Western blot were used to detect the expression of NRAGE mRNA and protein in CRC tumor cell lines HT29 , SW480 , SW620 , LOVO and colorectal normal cell line FHC. MTT proliferation experiment and Transwell migration experiment were used to observe the tumor cell proliferation and migration ability of the NC group , overexpression NRAGE group and NRAGE knockdown group. The expression differences of AKT , p ⁃AKT , ERK1/2 , p ⁃ERK1/2 , E ⁃cadherin , N ⁃cadherin and Vimentin were detected by qPCR and Western blot. Results : Compared with adjacent tissues , NRAGE mRNA and protein expression in CRC cancer tissues were significantly higher. The expression of NRAGE in cancer tissues was related to tumor stage , distant metastasis and lymph node metastasis (all P < 0. 05) . Compared with FHC cells , CRC tumor cell lines HT29 , SW480 , SW620 , and LOVO cells had higher NRAGE mRNA and protein expression (P < 0. 05) . Compared with the NC group , the proliferation and migration ability of CRC tumor cells in the overexpression NRAGE group was significantly enhanced , while the knockdown group was significantly weakened. Compared with the NC group , the SW480 cells in the overexpression NRAGE group had higher p ⁃ERK1/2 protein expression , but there was no significant difference in the expression of ERK1/2 , AKT and p ⁃AKT. After the SW480 cells in the overexpression NRAGE group were treated with ERK inhibitor U0126 , the proliferation and migration ability of SW480 cells significantly reduced. Methods NRAGE can promote the epithelial⁃mesenchymal transition of CRC cells and enhance the proliferation and migration of CRC tumor cells by activating ERK signaling pathway.