An Investigation into the Influence of ACTG2 on Gastric Cancer Prognosis and Cellular Biological Behaviors

Background This study investigates the impact of ACTG2 expression on poor prognosis in gastric cancer (GC) patients, as well as the biological behavior of GC cells. Methods Differential gene expression analysis was conducted on GC samples with distant metastasis and those without, utilizing the TCGA database. We constructed a protein interaction network for the differentially expressed genes and identified the target gene ACTG2. Subsequently, we explored the correlation between ACTG2 gene expression levels and prognosis, as well as clinical features. A GC cell line exhibiting significantly low ACTG2 expression was selected, and ACTG2 expression was upregulated using a human ACTG2 overexpression plasmid. The effects of ACTG2 on cancer cell proliferation, apoptosis, invasion, and migration were verified through CCK-8, flow cytometry, Transwell, and cell scratch assays. Results A total of 55 differentially expressed genes associated with distant metastasis of cancer were identified from the TCGA database. The expression of ACTG2 was significantly reduced in cancer tissues and showed a significant correlation with overall survival, progression-free survival, and post-progression survival of cancer patients. Further analysis confirmed that ACTG2 expression is positively correlated with the infiltration levels of CD8 ⁺ T cells, CD4 ⁺ T cells, neutrophils, monocytes, macrophages, and dendritic cells, demonstrating the potential role of ACTG2 in immune regulation. Notably, the ACTG2 gene is significantly downregulated in the cancer cell lines HGC-27 and AGS. After upregulating ACTG2 expression, the proliferation, invasion, and migration abilities of HGC-27 and AGS cells were significantly reduced, while their apoptosis ability was significantly enhanced. Conclusion The reduced expression of ACTG2 in gastric cancer (GC) may correlate with a poor prognosis, highlighting its potential significance as a prognostic biomarker. Furthermore, the overexpression of ACTG2 has been shown to inhibit the proliferation, migration, and invasion of GC cells, thereby underscoring its potential role in the pathogenesis and progression of GC.