ArticleeLife2021
Fine-tuned repression of Drp1-driven mitochondrial fission primes a 'stem/progenitor-like state' to support neoplastic transformation.
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- DNA base lesion-containing G-quadruplex mediates transcriptome reprogramming in EGFR-TKI resistance of non-small cell lung cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- The DRP1 receptor FIS1 is critical to the expansion of triple-negative breast cancer tumor-initiating cells.Cancer cell international · 2025Article
- Mitochondrial fusion and cristae reorganization facilitate acquisition of cardiomyocyte identity during reprogramming of murine fibroblasts.Cell reports · 2025Article
- Drp1 splice variants regulate ovarian cancer mitochondrial dynamics and tumor progression.EMBO reports · 2024Article
- Alternative splice variants of the mitochondrial fission proteinbioRxiv : the preprint server for biology · 2024Article
- Significance of quantitative analyses of the impact of heterogeneity in mitochondrial content and shape on cell differentiation.Open biology · 2024Review
- The LncRNA LENOX Interacts with RAP2C to Regulate Metabolism and Promote Resistance to MAPK Inhibition in Melanoma.Cancer research · 2022Article
- Drp1 regulates transcription of ribosomal protein genes in embryonic hearts.Journal of cell science · 2022Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Gene knockout of the master regulator of mitochondrial fission, Drp1, prevents neoplastic transformation. Also, mitochondrial fission and its opposing process of mitochondrial fusion are emerging as crucial regulators of stemness. Intriguingly, stem/progenitor cells maintaining repressed mitochondrial fission are primed for self-renewal and proliferation. Using our newly derived carcinogen transformed human cell model, we demonstrate that fine-tuned Drp1 repression primes a slow cycling 'stem/progenitor-like state', which is characterized by small networks of fused mitochondria and a gene-expression profile with elevated functional stem/progenitor markers (Krt15, Sox2 etc) and their regulators (Cyclin E). Fine tuning Drp1 protein by reducing its activating phosphorylation sustains the neoplastic stem/progenitor cell markers. Whereas, fine-tuned reduction of Drp1 protein maintains the characteristic mitochondrial shape and gene-expression of the primed 'stem/progenitor-like state' to accelerate neoplastic transformation, and more complete reduction of Drp1 protein prevents it. Therefore, our data highlights a 'goldilocks' level of Drp1 repression supporting stem/progenitor state dependent neoplastic transformation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.