ArticleOxidative medicine and cellular longevity2022
TRIM65 Promotes Malignant Cell Behaviors in Triple-Negative Breast Cancer by Impairing the Stability of LATS1 Protein.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- TRIM Protein Superfamily in Breast Cancer: Yin and Yang.Biochemical genetics · 2026Review
- The Magic and Mystery of TRIM65 in Diseases.Current medicinal chemistry · 2025Review
- Cancer-associated fibroblasts affect breast cancer cell sensitivity to chemotherapeutic agents by regulating NRBP2.Toxicology research · 2024Article
- Addressing the mean-variance relationship in spatially resolved transcriptomics data withbioRxiv : the preprint server for biology · 2024Article
- TRIM65 deficiency alleviates renal fibrosis through NUDT21-mediated alternative polyadenylation.Cell death and differentiation · 2024Article
- Multifaceted role ofMedComm · 2024Review
- TRIM65/NF2/YAP1 Signaling Coordinately Orchestrates Metabolic and Immune Advantages in Hepatocellular Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- TRIM65 promotes renal cell carcinoma through ubiquitination and degradation of BTG3.Cell death & disease · 2024Article
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Authors and funding
10 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
TNBC is a malignant tumor that easily relapses and metastasizes, with a poor prognosis in women. Ubiquitination plays a key role in promoting the tumor process. In various tumors, TRIM65 can affect malignant biological tumor behavior by ubiquitination of related proteins. We aimed to investigate TRIM65 expression in TNBC and whether it promotes malignant biological behavior in TNBC cells using Cell Counting Kit-8, colony formation, and transwell assays. Mechanically, we confirmed that TRIM65 promoted TNBC invasion and metastasis by ubiquitination of LATS1 protein through Co-IP, CHX, and endogenous ubiquitination experiments. The expression of TRIM65 was abnormally high and accelerated the proliferation, invasion, and migration of MDA-MB-231 and MDA-MB-453 cells.
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Registered trials
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