Exploring the Molecular Mechanisms and Biological Effects of CELF2 in the Development of Gastric Cancer.

[INTRODUCTION] The CUGBP ELAV-like family member 2 (CELF2) gene is irregularly expressed in various types of cancer. However, the role of CELF2 in stomach adenocarcinoma (STAD) remains unclear. This study aims to elucidate its potential role in modulating tumor behavior in STAD, as well as its correlation with tumor-infiltrating immune cells.

[METHODS] Bioinformatics analysis methods were employed to investigate the CELF2 expression levels of CELF2 in STAD and its correlation with clinicopathological factors. CELF2 expression was quantified in STAD cells using qRT-PCR and Western blot. Immunohistochemistry confirmed CELF2 expression in STAD versus adjacent normal tissues. The effects of CELF2 expression on cell proliferation were evaluated using CCK-8 and colony formation assays, and migration and invasion assays evaluate cellular motility and invasiveness. Differential expression and protein-protein interaction (PPI) network analysis were conducted to predict the downstream targets of CELF2.

[RESULTS] Our findings revealed that CELF2 expression was significantly reduced in STAD tissues and was correlated with patient survival outcomes. Moreover, CELF2 overexpression demonstrated a notable inhibitory effect on cell proliferation, migration, and invasion in STAD cells. Importantly, CELF2 appeared to exert its effects through the regulation of the downstream target gene adiponectin (ADIPOQ). The knockdown of ADIPOQ effectively negated the inhibitory effects of CELF2 on cell proliferation and migration.

[DISCUSSION] This study underscores CELF2 as a tumor suppressor in STAD, whose downregulation promotes progression and correlates with poor prognosis. The CELF2/ADIPOQ axis represents a new regulatory pathway with therapeutic implications. The lack of deeper mechanistic insights into how CELF2 regulates ADIPOQ also warrants further investigation.

[CONCLUSION] CELF2 acts as a tumor suppressor in STAD by inhibiting proliferation, migration, and invasion, partly through regulating ADIPOQ and influencing the immune microenvironment. It represents a promising prognostic biomarker and new therapeutic target, with the CELF2/ADIPOQ axis offering a specific pathway for future drug development.