EFFECT AND MECHANISM OF LNCRNA PVT1 ON PROLIFERATION, MIGRATION, INVASION AND AUTOPHAGY OF GASTRIC CANCER CELLS

Lan Pang¹, Cancan Liang², Jiang Wu¹, Peng Chen¹, Wenjing Ji^{2, *}

¹Department of the Endoscopic Diagnosis and Treatment, The Second Affiliated Hospital of Xinjiang Medical University, Urumqi 830000, PR China - ²Department of Digestive Internal Medicine, The Second Affiliated Hospital of Xinjiang Medical University, Urumqi 830000, PR China

Objective: To explore the mechanisms underlying the effects of the long non-coding RNA plasmacytoma variant translocation 1 (LncRNA PVT1) on the proliferation, migration, invasion, and autophagy of gastric cancer cells. 

Methods: The human gastric cancer cell line SGC-7901 was cultured in vitro, and gastric cancer cells were transfected with an LncRNA PVT1 overexpression vector, an LncRNA PVT1 silencing vector, or the corresponding control vectors, resulting in an LncRNA PVT1 overexpression group, an overexpression control group, an LncRNA PVT1 knockout group, and a knockout control group. Cell proliferation was detected by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, cell migration and invasion were detected by Transwell assay, autophagy-related 5 (ATG5), and large tumor suppressor kinase 2 (LATS2) protein expression was detected by Western blot assay, and LATS2 mRNA expression was detected by real-time quantitative PCR assay. 

Results: The LncRNA PVT1 overexpression group and the overexpression control group significantly promoted the proliferation, migration, and invasion of gastric cancer cells at each time point assessed (P<0.05). The LncRNA PVT1 knockout group and the knockout control group displayed significant inhibitory effects against cell proliferation, migration, and invasion at each time point assessed (P<0.05). The expression of ATG5 protein was significantly increased in the LncRNA PVT1 overexpression group compared with that in the overexpression control group (P<0.05). The expression of ATG5 protein was significantly reduced in the LncRNA PVT1 knockout group compared with that in the knockout control group (P<0.05). The expression levels of both LATS2 mRNA and protein significantly decreased in the LncRNA PVT1 overexpression group compared with those in the overexpression control group (P<0.05). LATS2 mRNA and protein expression levels were significantly increased in the LncRNA PVT1 knockout group compared with the knockout control group (P<0.05). 

Conclusion: LncRNA PVT1 was able to promote the proliferation, migration, and invasion of gastric cancer cells, which may be associated with the regulation of LATS2 expression. LncRNA PVT1 directly affected cellular autophagy by upregulating ATG5 protein expression.