ArticleJournal of molecular histology2026
MUL1 suppresses cervical cancer progression by targeting FUNDC1 for ubiquitination and inhibiting DRP1-dependent mitophagy.
Article in Journal of molecular histology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Authors and funding
4 authors.
Funding
Abstract
Cervical cancer is the fourth most common cancer in women worldwide. Mitochondrial E3 ubiquitin ligase 1 (MUL1) plays a crucial role in cancer processes, yet its role in cervical cancer remains unclear. Here, we observed that MUL1 mRNA and protein levels were reduced in cervical cancer tissues and cells using qRT-PCR and Western blot assays. Patients with low MUL1 expression exhibited poor survival. CCK-8, EdU, Transwell and flow cytometry analysis demonstrated that MUL1 overexpression inhibited cervical cancer cell proliferation and migration and promoted cell apoptosis, while MUL1 knockdown had opposite effects. Interestingly, inhibition of mitophagy induced by Midivi-1 attenuated the effects of MUL1 knockdown on cell proliferation, migration, and apoptosis. Mechanistically, co-immunoprecipitation and ubiquitination assays demonstrated that MUL1 decreased FUN14 domain containing 1 (FUNDC1) protein stability by promoting its ubiquitination. FUNDC1 overexpression promoted dynamin-related protein 1 (DRP1) expression and promoted mitophagy in cervical cancer cells, whereas DRP1 knockdown reversed these changes. Notably, FUNDC1 knockdown weakened the promoting effects of MUL1 knockdown on mitophagy. FUNDC1 overexpression rescued the inhibitory effects on proliferation, migratory capacity and the promoting effect on apoptosis. In vivo, MUL1 overexpression inhibited tumor growth in a xenograft mouse model. These findings suggested MUL1 suppressed cervical cancer progression by targeting the FUNDC1/DRP1 axis and inhibiting mitophagy, highlighting its potential as a therapeutic target.
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