The CADM2/Akt pathway is involved in the inhibitory effect of miR-21-5p downregulation on proliferation and apoptosis in esophageal squamous cell carcinoma cells.

Esophageal squamous cell carcinoma (ESCC), the main subtype of esophageal cancer, is the eighth most common cancer worldwide. Cell adhesion molecule 2 (CADM2) has been reported to be a tumor suppressor and is usually downregulated in several cancers. However, the role of CADM2 in ESCC remains unknown. The aim of the present study was to evaluate the potential role and underlying action mechanism of CADM2 in ESCC. Herein, we found that CADM2 was low-expressed in ESCC tissues and cell lines. CADM2 overexpression inhibited proliferation and induced apoptosis of ESCC cells. Moreover, CADM2 overexpression also suppressed the Akt signaling pathway in ESCC cells. MiR-21-5p down-regulation inhibited cell proliferation and induced cell apoptosis, while CADM2 knockdown attenuated the effect of anti-miR-21-5p. The expression of p-Akt was decreased in the cells transfected with anti-miR-21. However, the expression of p-Akt was increased in the cells co-transfected with anti-miR-21-5p and si-CADM2 compared with that in anti-miR-21-5p-transfecting cells. In summary, the CADM2/Akt pathway is involved in the inhibitory effect of miR-21-5p downregulation on proliferation and apoptosis in ESCC cells. These findings indicated that the miR-21-5p/CADM2/Akt axis might be a new approach for the treatment of ESCC.