FAM107A demonstrates reduced invasion in colorectal cancer, indicating possible regulatory mechanisms through EMT and AKT pathway.
Metastasis of colorectal cancer (CRC) is the main cause of CRC-related mortality. FAM107A is widely expressed in various normal tissues. However, few studies have revealed the biological function of FAM107A in epithelial-mesenchymal transition (EMT) in human cancer cells, and the related molecular mechanisms and signaling cascades are completely unknown. Here, we found that FAM107A was abnormally expressed in human CRC tissues and cell lines. Further research has shown that overexpression of FAM107A through transfection weakened the expression level of EMT-related markers. In addition, our research results indicated that upregulation of FAM107A inhibited the AKT signaling cascade in human CRC cells, while AKT activators restored activation of p50, indicating that FAM107A may regulate EMT through AKT activation of p50. Our results suggest that FAM107A could be a potential target for the treatment of CRC.
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Chen et al. (2025) studied this question.
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