Up-regulation of collagen type V alpha 2 (COL5A2) promotes malignant phenotypes in gastric cancer cell via inducing epithelial-mesenchymal transition (EMT)

Recent studies have reported that collagen type V alpha 2 (COL5A2) is a hub gene and associated with the prognosis of gastric cancer (GC) patients, playing an important role in GC. In this study, we aim to fathom out the biological roles of COL5A2 and its relevant mechanism in GC. Oncomine, gene expression profiling interactive analysis, and UALCAN were used to explore the effects of COL5A2 on GC. Cell counting kit-8 assay, colony formation assay, and transwell assay were conducted to investigate the biological behaviors of GC cell lines AGS and SGC-7901. Quantitative reverse transcription polymerase chain reaction and western blot were performed to determine gene and protein expressions. COL5A2 expression was up-regulated and negatively correlated with survival percentage of GC patients. COL5A2 expression was notably elevated in high stage and high grade of GC. Down-regulation of COL5A2 inhibited proliferation, migration, and invasion of AGS and SGC-7901 cells. COL5A2 induced epithelial-mesenchymal transition (EMT) by promoting the expressions of mesenchymal markers (SNAI1, SNAI2, TWIST, VIM, and MMP2), thereby facilitating the malignant phenotypes of GC. COL5A2 plays an oncogenic role in GC and has potential to predict the progression and prognosis of GC patients.

Automated summary

Recent studies have found that COL5A2, a hub gene, is associated with the prognosis of gastric cancer patients and plays a crucial role in gastric cancer. This study aimed to investigate the biological functions of COL5A2 and its mechanism in gastric cancer. The expression of COL5A2 was up-regulated and negatively correlated with survival percentage in gastric cancer patients. COL5A2 expression was significantly increased in high stage and high grade gastric cancer. Down-regulation of COL5A2 inhibited the proliferation, migration, and invasion of gastric cancer cells. COL5A2 induced epithelial-mesenchymal transition and facilitated the malignant phenotypes of gastric cancer by promoting the expressions of mesenchymal markers.