Loss of TPM1 Promotes Colorectal Cancer Proliferation and Metastasis by Inducing Epithelial-Mesenchymal Transition and Regulating Cytoskeletal Remodeling

Abstract

Background: Tropomyosin 1 (TPM1) is an important actin-binding protein and has been identified as a tumor suppressor in various malignant tumors. However, the role of TPM1 in colorectal cancer remains to be explored. This study aimed to clarify the specific function and mechanism of TPM1 in colorectal cancer. Methods: To investigate the effect of TPM1 on cell proliferation, migration, and invasion, we constructed cell models with TPM1 knockdown and overexpression. Cytoskeletal changes were observed by phalloidin staining, and changes in epithelial-mesenchymal transition (EMT) markers were detected by Western blot. Results: This study revealed that TPM1 expression was decreased in human colorectal cancer. Downregulation of TPM1 promoted cell migration, invasion, and proliferation. Moreover, loss of TPM1 decreased the stability of the cytoskeleton. Overexpression of TPM1 significantly inhibited the EMT process of colorectal cancer cells, while downregulation of TPM1 significantly promoted this key process involved in tumor metastasis. Conclusions: The results showed that downregulation of TPM1 promotes colorectal cancer progression. The underlying mechanism may involve the reduction in actin stability, cytoskeletal rearrangement, and enhancement of cell migration and EMT.