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Study of effects and mechanism of long non-coding RNA FAL1 on the proliferation and apoptosis of gastric cancer cells |
CAO Xiankui XIE Bin SHAO Yang LIN Jie |
Departmen of General Surgery, Liaoning Cancer Hospital & Institute, Liaoning Province, Shenyang 110042, China |
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Abstract Objective To explore the effect and mechanism of long non-coding RNA FAL1 on the proliferation and apoptosis of gastric cancer. Methods Normal gastric mucosal cells GES-1 and gastric cancer cells SGC-7901, BGC-823 were taken from the Central Laboratory of Liaoning Cancer Hospital & Institute, and RT-PCR was used to detect the expression of FAL1 and STAT3 in the cells; Western-blot was detected the expression of STAT3 protein; inhibition of FAL1 and overexpression of STAT3 in gastric cancer cells, double staining with CCK-8 and Annexin V-FITC PI were evaluated cell proliferation and apoptosis. Results The expression levels of FAL1 in human gastric cancer cell lines SGC-7901 and BGC-823 were higher than that in gastric mucosal cells GES-1, and the differences were statistically significant (P < 0.05). The expression levels of STAT3 in SGC-7901 and BGC-823 were higher than that in GES-1, and the differences were statistically significant (P < 0.05). The expression level of FAL1 in gastric cancer cells was decreased after transfection (P < 0.05). The expression level of STAT3 in gastric cancer cells was also decreased (P < 0.05). After the si-FAL1#2 sequence was transfected into SGC-7901 and BGC-823 cells, cell proliferation was slowed down. On this basis, over-expression of STAT3, the proliferation ability of the inhibited cells was partially restored (P < 0.05); early cell apoptosis increased significantly, after overexpression of STAT3, apoptotic cells were decreased (P < 0.05). Conclusion FAL1 promotes the proliferation of gastric cancer cells and inhibits apoptosis by up-regulating the expression of STAT3.
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