LncRNA SNHG7 promotes the proliferation and inhibits apoptosis of gastric cancer cells by repressing the P15 and P16 expression

M.-W. Wang, J. Liu, Q. Liu, Q.-H. Xu, T.-F. Li, S. Jin, T.-S. Xia

Department of Pathology, Hubei Cancer Hospital, Wuhan, China. xtszx@sina.com

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• Oncology

OBJECTIVE: To investigate the relative expression of long non-coding small nucleolar RNA host gene 7 (lncRNA SNHG7) in gastric cancer tissues and cells, the effect of lncRNA SNHG7 on proliferation and apoptosis of gastric cancer cells in vivo and in vitro experiments, and the relevant mechanism.

PATIENTS AND METHODS: Real-time quantitative polymerase chain reaction (qRT-PCR) experiment was performed to detect the relative expressions of SNHG7 in the gastric cancer tissues and cells. In presence of lip2000, SNHG7 interference sequence was transiently transfected into the gastric cancer cells followed by transfection efficiency detection by qRT-PCR. Cell count kit 8 (CCK-8) and clone formation assay were also carried out to detect the effect of SNHG7 on the proliferation of gastric cancer cells, flow cytometry (FCM) to detect the effect of SNHG7 on the cycle and apoptotic rate of gastric cancer cells, in vivo experiment to detect the effect of SNHG7 on biological behaviors of gastric cancer cells, and Western blotting assay to detect the variations in expression of downstream proteins after SNHG7 expression was interfered.

RESULTS: The qRT-PCR experiment showed that in a total of 68 cases of cancer tissues and tumor-adjacent tissues, the relative expression of SNHG7 was upregulated in 48 cases of gastric cancer tissues and 5 gastric cancer cell lines. The in vitro experiments showed that after SNHG7 expression was interfered, the proliferation of gastric cancer cells was inhibited with an increase in apoptotic rate and arrest of cell cycle in G1/G0 phase. Experiment on nude-mouse transplanted tumor model confirmed that after SNHG7 expression was interfered, in vivo tumor growth was inhibited, and the Western blotting assay revealed that regulation of p15 and p16 expressions constituted a part of the potential molecular mechanism.

CONCLUSIONS: Relative expression of SNHG7 is upregulated in gastric cancer tissues and cells, and partially contributes to the development and progression of gastric cancer through regulation of p15 and p16 expressions. Thus, interference on expression of SNHG7 can provide critical the theoretical basis for inverting the malignant phenotype of gastric cancer in clinical practice.

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