Silencing of Acyl-CoA Thioesterase 7 Inhibits Proliferation and Metastatic Potential in Colorectal Cancer Cells

Acyl-CoA thioesterase 7 (ACOT7) has emerged as a candidate gene implicated in various malignancies. However, its functional relevance in colorectal cancer (CRC) remains poorly understood.

To investigate the role of ACOT7 in CRC, we examined its expression in normal colon epithelial cells and a panel of CRC cell lines using quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting. Functional analyses were performed following siRNA-mediated knockdown of ACOT7 to assess changes in cell proliferation, clonogenicity, cell cycle distribution, apoptosis, migration, and invasion using MTT, colony formation, flow cytometry, and Transwell-based assays.

ACOT7 was markedly over-expressed at both the mRNA and protein levels in CRC cells compared to normal epithelial cells. Silencing ACOT7 substantially reduced cell proliferation and clonogenic potential. Flow cytometric analysis indicated cell cycle arrest and an increase in the sub-G₀/G₁ population, indicative of apoptosis in ACOT7-depleted cells. Furthermore, suppression of ACOT7 substantially impaired both cell migration and invasion, suggesting its key role in metastatic progression.

These findings highlight ACOT7 as a critical regulator of the proliferation, survival, and metastatic potential of CRC cells and support its candidacy as a potential therapeutic target for colorectal malignancies.