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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

Transmembrane and coiled-coil domains 1 (TMCO1) is a recently discovered transmembrane protein of endoplasmic reticulum (ER), which plays a critical role in maintaining calcium homeostasis. TMCO1 dysfunction has been proved to be closely related to a variety of human diseases, including glaucoma, deformities, mental retardation and tumorigenesis. However, the role of TMCO1 in gliomas remains unclear. The purpose of this study was to detect the role of TMCO1 in the pathogenesis and progression of gliomas. This study demonstrated that TMCO1 was upregulated in gliomas and its overexpression predicted poor prognosis. We also revealed that the expression of TMCO1 was associated with the World Health Organization (WHO) grade of gliomas. Knockdown of TMCO1 inhibited the proliferation and induced apoptosis of U87 and U251 cells. In addition, TMCO1 induced GBM cell migration and invasion by promoting epithelial-mesenchymal transition (EMT). These date collectively proved the crucial role of TMCO1 as a novel prognostic factor and underlying therapeutic target for glioma patients. [ABSTRACT FROM AUTHOR]