LncRNA LOC100507144 Predicts Poor Clinical Outcomes and Regulates Tumor Progress in Gastric Cancer

Abstract

Background: The enhanced proliferation and invasiveness of cancer cells have been associated with the pathophysiology of gastric cancer (GC). However, the precise role of the regulatory system has yet to be identified. The primary objective of this investigation was to ascertain the potential involvement of LOC100507144, a long non-coding RNA, in the pathogenesis of GC. Method: A total of 370 gastric cancer cases were collected for this study. GC cell lines were cultured and authenticated. Gene knockdown and overexpression were achieved using siRNAs and lentivirus. RT-qPCR was performed to assess gene expression. Clonogenic assay, immunohistochemistry, invasion assay, and Western blot were conducted. The dual-luciferase reporter gene assay was utilized to investigate mRNA target binding. Moreover, to simulate the aggressive in vivo behavior of GC, the cell lines BGC-823 and MGC-803 were used. Gain and loss of function studies examined cell proliferation and invasion. Results: LOC100507144 expression was substantially higher in GC tissues than in neighboring normal tissues, and this elevation was linked with tumor pathogenesis. In vitro studies demonstrated that LOC100507144 overexpression significantly increased cell proliferation and invasion, whereas LOC100507144 knockdown suppressed these effects. The expression of the enzyme phospholysine phosphohistidine inorganic pyrophosphate phosphatase (LHPP) was considerably lower in adjacent tissues, which was inversely related to the stage of GC. The LOC100507144, as per the in vitro assay, regulated LHPP expression and encouraged the GC onset and progression. Conclusions: In summary, the present investigation has determined that the upregulation of LOC100507144 leads to the downregulation of LHPP expression, promoting the advancement of GC.