ABSTRACT
Long non-coding RNA KCNQ1OT1 is highly expressed in a variety of tumors, but there are few studies in gastric cancer and the results are inconsistent. The relevant research of its specific mechanism in gastric cancer is also scarce. Through the analysis of several TCGA public databases, we found that KCNQ1OT1 was generally highly expressed in gastric cancer, and the prognosis of gastric cancer patients with a high expression of KCNQ1OT1 was poor. The expression of KCNQ1OT1 is closely related to many clinical factors of gastric cancer, especially the mutation of TP53, and its expression is significantly related to immune cell infiltration. KCNQ1OT1 is generally highly expressed in gastric cancer cell lines. Knockdown of KCNQ1OT1 can inhibit the proliferation of gastric cancer cell lines. Co- expression network analysis showed that its expression was closely related to tumor metabolism. Glutaminase 1 (GLS1) is generally highly expressed in gastric cancer, which is closely related to a poor prognosis. There is a significant correlation between the expression of KCNQ1OT1 and GLS1. Knockdown of KCNQ1OT1 can inhibit the expression of GLS1 mRNA, and overexpression of GLS1 can partially rescue the proliferation of gastric cancer cells caused by knockdown of KCNQ1OT1. Therefore, we speculate that KCNQ1OT1 may regulate the growth of gastric cancer cells through GLS1. Our study explored the role of KCNQ1OT1 in gastric cancer through bioinformatics database and experiments, suggesting that KCNQ1OT1 may promote the development of gastric cancer by regulating glutamine metabolism, which provides a new target for the clinical research on targeted treatment in gastric cancer.