ArticleMolecular therapy : the journal of the American Society of Gene Therapy2022
Mitochondrial fragmentation is crucial for c-Myc-driven hepatoblastoma-like liver tumors.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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25 citing papers in PubMed, 30 citations in OpenAlex.
- Reactivation of DRP1 plays a functional role in resistance to MEK inhibition in pancreatic cancer cells.British journal of cancer · 2026Article
- Hyperbaric Oxygen Attenuates Cerebral Ischemia-Reperfusion Injury Through ROS-Dependent Remodeling of Microglial Mitochondrial Dynamics.International journal of molecular sciences · 2026Article
- Review
- Reactivation of DRP1 plays a functional role in resistance to MEK inhibition in pancreatic cancer cells.bioRxiv : the preprint server for biology · 2026Article
- Imbalances of mitochondrial dynamics in solid tumors.Oncogenesis · 2026Review
- Arginine dependency in omental metastasis of epithelial ovarian cancer reveals a therapeutic vulnerability.Cell death & disease · 2026Article
- Mitochondrial fission and fusion in inflammatory diseases: mechanisms and therapeutic implications.Journal of translational medicine · 2025Review
- Mitochondrial dysfunction in hepatocellular carcinoma: from metabolism to targeted therapies.Molecular and cellular biochemistry · 2025Review
- SKP2 ubiquitylation modifies IDH1 to regulate hepatoblastoma cell cycle and glucose metabolism.BMC cancer · 2025Article
- Relationship Between Total Parenteral Nutrition, Ventilation, and Hepatoblastoma: A Study of 258,929 Neonatal Intensive Care Unit Admissions.Pediatric blood & cancer · 2025Article
- DRP1, fission and apoptosis.Cell death discovery · 2025Review
- Hepatoblastoma: From Molecular Mechanisms to Therapeutic Strategies.Current oncology (Toronto, Ont.) · 2025Review
- Targeting the epigenome and tumor heterogeneity: advances in immunotherapy for chemoresistant metastatic colorectal cancer.Frontiers in immunology · 2025Review
- Ubiquitin regulatory X (UBX) domain-containing protein 6 is essential for autophagy induction and inflammation control in macrophages.Cellular & molecular immunology · 2024Article
- LASS2 enhances p53 protein stability and nuclear import to suppress liver cancer progression through interaction with MDM2/MDMX.Cell death discovery · 2023Article
- Review
- BEX1 supports the stemness of hepatoblastoma by facilitating Warburg effect in a PPARγ/PDK1 dependent manner.British journal of cancer · 2023Article
- Small mitochondrial protein NERCLIN regulates cardiolipin homeostasis and mitochondrial ultrastructure.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Sp1 promotes tumour progression by remodelling the mitochondrial network in cervical cancer.Journal of translational medicine · 2023Article
- Hydrodynamic Delivery: Characteristics, Applications, and Technological Advances.Pharmaceutics · 2023Review
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatoblastoma is the most common liver cancer in children, and the aggressive subtype often has a poor prognosis and lacks effective targeted therapy. Although aggressive hepatoblastoma (HB) is often accompanied by abnormally high expression of the transcription factor c-Myc, the underlying mechanism remains unclear. In this study, we found that mitochondrial fragmentation was enhanced by c-Myc overexpression in human aggressive HB tissues and was associated with poor prognosis. Then, a mouse model resembling human HB was established via hydrodynamic injection of c-Myc plasmids. We observed that liver-specific knockout of the mitochondrial fusion molecule MFN1 or overexpression of mitochondrial fission molecule DRP1 promoted the occurrence of c-Myc-driven liver cancer. In contrast, when MFN1 was overexpressed in the liver, tumor formation was delayed. In vitro experiments showed that c-Myc transcriptionally upregulated the expression of DRP1 and decreased MFN1 expression through upregulation of miR-373-3p. Moreover, enhanced mitochondrial fragmentation significantly promoted aerobic glycolysis and the proliferation of HB cells by significantly increasing reactive oxygen species (ROS) production and activating the RAC-alpha serine/threonine-protein kinase (AKT)/mammalian target of rapamycin (mTOR) and nuclear factor κB (NF-κB) pathways. Taken together, our results indicate that c-Myc-mediated mitochondrial fragmentation promotes the malignant transformation and progression of HB by activating ROS-mediated multi-oncogenic signaling.
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