关键词: 宫颈癌, TMCO1, 增殖, 迁移

Abstract:

Background and purpose: Transmembrane and coiled-coil domains 1 (TMCO1) is a recently discovered endoplasmic reticulum calcium channel protein that has been found to be associated with the progression of various tumors, however, its role in cervical cancer has not yet been clarified. This study aimed to investigate the effects of TMCO1 on the proliferation and migration of cervical cancer HeLa cells. Methods: By transfecting cervical cancer HeLa cells with plasmids, cells with stable overexpression of TMCO1 and cells with stable knockdown of TMCO1 were obtained. Cell counting kit-8 (CCK-8) assay, clone formation assay and EdU labeling assay were used to detect cell proliferation ability, transwell assay was used to detect cell migration ability, and proteomic analysis was performed on the cells that stably overexpressed TMCO1 and control cells. Results: TThe CCK-8 experiment and clone formation experiment showed that overexpression of TMCO1 in cervical cancer HeLa cells significantly increased their proliferation ability (P<0.05). EdU labeling experiments showed that overexpression of TMCO1 in cervical cancer HeLa cells significantly increased the number of cells undergoing active DNA synthesis (P<0.01). After knocking down TMCO1 in cervical cancer HeLa cells, the expression of cell cycle inhibitory protein p27 increased, and the phosphorylation of histone H3 decreased. Clonogenesis experiments showed that knocking down TMCO1 significantly inhibited the proliferation of cervical cancer HeLa cells (P<0.001). EdU labeling experiments showed that after knocking down TMCO1 in cervical cancer HeLa cells, the number of cells undergoing active DNA synthesis was significantly reduced (P<0.05). Transwell experiment showed that overexpression of TMCO1 in cervical cancer HeLa cells significantly increased their migration ability (P<0.001), while knocking down TMCO1 significantly inhibited the migration of cervical cancer HeLa cells (P<0.001). The pathways related to extracellular matrix adhesion and PI3K-AKT signaling were significantly upregulated in the cells with stable overexpression of TMCO1, while ribosome related pathways were downregulated in proteomic analysis. Conclusion: Overexpression of TMCO1 significantly promotes the proliferation and migration of cervical cancer cells, while knockdown of TMCO1 significantly inhibits the proliferation and migration of cervical cancer HeLa cells. TMCO1 may affect the proliferation and migration of HeLa cells by regulating cell adhesion and signal transduction.

Key words: Cervical cancer, TMCO1, Proliferation, Migration