ArticleCancer gene therapy2023
TMTC1 promotes invasiveness of ovarian cancer cells through integrins β1 and β4.
Article in Cancer gene therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Genetic attenuation of ALDH1A1 increases metastatic potential and aggressiveness in colorectal cancer.Molecular oncology · 2026Article
- Sweet Surprises: Decoding Tumor-Associated Glycosylation in Cancer Progression and Therapeutic Potential.Cells · 2026Review
- Transcriptome and single-cell RNA sequencing analysis with 101 machine learning combinations and experimental verification reveals the mechanism of action of mannose metabolism in bladder cancer.Frontiers in immunology · 2026Article
- Establishment of a Predictive Model for Mortality in Sepsis Patients Using WGCNA and Machine Learning Algorithms.Journal of inflammation research · 2026Article
- Diagnostic value of C-reactive protein/ albumin ratio and TMTC1 in intracranial atherosclerotic stenosis in patients with acute cerebral infarction.Scientific reports · 2025Article
- Prognostic value ofHeliyon · 2024Article
- Protein O-mannosylation: one sugar, several pathways, many functions.Glycobiology · 2023Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Ovarian cancer is the most lethal gynecological malignancy and is characterized by peritoneal disseminated metastasis. Although O-mannosyltransferase TMTC1 is highly expressed by ovarian cancer, its pathophysiological role in ovarian cancer remains unclear. Here, immunohistochemistry showed that TMTC1 was overexpressed in ovarian cancer tissues compared with adjacent normal ovarian tissues, and high TMTC1 expression was associated with poor prognosis in patients with ovarian cancer. Silencing TMTC1 reduced ovarian cancer cell viability, migration, and invasion in vitro, as well as suppressed peritoneal tumor growth and metastasis in vivo. Moreover, TMTC1 knockdown reduced cell-laminin adhesion, which was associated with the decreased phosphorylation of FAK at pY397. Conversely, TMTC1 overexpression promoted these malignant properties in ovarian cancer cells. Glycoproteomic analysis and Concanavalin A (ConA) pull-down assays showed that integrins β1 and β4 were novel O-mannosylated protein substrates of TMTC1. Furthermore, TMTC1-mediated cell migration and invasion were significantly reversed by siRNA-mediated knockdown of integrin β1 or β4. Collectively, these results suggest that TMTC1-mediated invasive behaviors are primarily through integrins β1 and β4 and that TMTC1 is a potential therapeutic target for ovarian cancer.
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