CAP2 contributes to tumorigenesis in gastric cancer by targeting transcription factor SOX9.

Abstract

Gastric cancer (GC) is one of the most common tumors and the major cause of cancer-related mortality in the world. The purpose of this study is to identify new biomarker and reveal its potential molecular mechanism in GC. The expression of CAP2 was observed by the bioinformatics analysis and western blot assays. The effects of CAP2 on cell proliferation and growth were tested by MTT assay, EdU assay, colony formation assay, and flow cytometric assay, respectively. ChIP and dual-luciferase assays were confirmed that SOX9 binding sites were putative regulatory elements in the transcriptional activation of CAP2. Furthermore, western blot and xenograft assays were applied to examine whether SOX9 was involved in the regulation of CAP2 expression. We reported that CAP2 is overexpressed in GC cells and tissues and related to a poorer prognosis for GC patients. Moreover, we found that knockdown of CAP2 suppressed the proliferation, growth, and cell cycle of GC cells. Besides, the transcription factor SOX9 participated in the CAP2-mediated proliferation of GC cells in vitro and in vivo. Our results provide novel evidence that CAP2 plays an essential role in the genesis and development of GC, thus potentially highlighting this gene as a therapeutic target.