Down-regulation of ACSM3 Promotes Tumorigenesis in Breast Cancer

Background/Aim: Breast cancer is one of the most frequently diagnosed cancers worldwide. This study aimed to investigate the biological function and clinical significance of acyl-CoA synthetase medium-chain family member 3 (ACSM3) in breast cancer.

Materials and Methods: RNA-seq data analysis was performed to evaluate ACSM3 expression in breast cancer tissues compared with normal breast tissues. Functional studies, including migration and invasion assays in vitro, as well as orthotopic xenograft models in vivo, were conducted to assess the role of ACSM3 in breast cancer progression.

Results: ACSM3 expression was significantly reduced in tumor tissues compared with normal breast tissues, with down-regulation observed in approximately 75% of cases. Over-expression of ACSM3 suppressed breast cancer cell migration and invasion and was associated with increased AKT phosphorylation. In xenograft models, ACSM3 over-expression inhibited tumor growth and metastatic potential.

Conclusion: ACSM3 functions as a tumor suppressor in breast cancer by regulating the WNT/AKT signaling pathway, thereby inhibiting cell proliferation, migration, and invasion. These results suggest that ACSM3 may serve as a potential therapeutic target for breast cancer treatment.