ArticleThe Journal of biological chemistry2017
Sequential adaptive changes in a c-Myc-driven model of hepatocellular carcinoma.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
43 citing papers in PubMed, 59 citations in OpenAlex.
- Reversible dissociation of mitochondrial Complex V balances anabolic and energy-generating needs in cancer.iScience · 2026Article
- Oncogenic function and transcriptional dynamics of MYCN in liver tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Review
- Derivation of Genetically Defined Murine Hepatoblastoma Cell Lines with Angiogenic Potential.Cancers · 2025Article
- MYC Binding Near Transcriptional End Sites Regulates Basal Gene Expression, Read-Through Transcription, and Intragenic Contacts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Gas1-Mediated Suppression of Hepatoblastoma Tumorigenesis.The American journal of pathology · 2025Article
- Article
- Fueling the fire-a pan-cancer analysis of MYC-regulated lipid metabolism.Frontiers in cell and developmental biology · 2025Review
- Body-Wide Inactivation of the Myc-Like Mlx Transcription Factor Network Accelerates Aging and Increases the Lifetime Cancer Incidence.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Partial Hepatectomy Promotes the Development of KRASG12V-Induced Hepatocellular Carcinoma in Zebrafish.Cancers · 2024Article
- An adenosine derivative promotes mitochondrial supercomplexes reorganization and restoration of mitochondria structure and bioenergetics in a diethylnitrosamine-induced hepatocellular carcinoma model.Scientific reports · 2024Article
- The Myc-Like Mlx Network Impacts Aging and Metabolism.bioRxiv : the preprint server for biology · 2023Article
- Premature aging and reduced cancer incidence associated with near-complete body-wide Myc inactivation.Cell reports · 2023Article
- A Novel Transgenic Mouse Model ImplicatesInternational journal of molecular sciences · 2023Article
- Targeting STEAP1 as an anticancer strategy.Frontiers in oncology · 2023Review
- Glutamine metabolic reprogramming in hepatocellular carcinoma.Frontiers in molecular biosciences · 2023Review
- Lessons in aging from Myc knockout mouse models.Frontiers in cell and developmental biology · 2023Review
- Disruption of Multiple Overlapping Functions Following Stepwise Inactivation of the Extended Myc Network.Cells · 2022Article
- Regulation of Normal and Neoplastic Proliferation and Metabolism by the Extended Myc Network.Cells · 2022Review
- Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Hepatocellular carcinoma (HCC) is a common cancer that frequently overexpresses the c-Myc (Myc) oncoprotein. Using a mouse model of Myc-induced HCC, we studied the metabolic, biochemical, and molecular changes accompanying HCC progression, regression, and recurrence. These involved altered rates of pyruvate and fatty acid β-oxidation and the likely re-directing of glutamine into biosynthetic rather than energy-generating pathways. Initial tumors also showed reduced mitochondrial mass and differential contributions of electron transport chain complexes I and II to respiration. The uncoupling of complex II's electron transport function from its succinate dehydrogenase activity also suggested a mechanism by which Myc generates reactive oxygen species. RNA sequence studies revealed an orderly progression of transcriptional changes involving pathways pertinent to DNA damage repair, cell cycle progression, insulin-like growth factor signaling, innate immunity, and further metabolic re-programming. Only a subset of functions deregulated in initial tumors was similarly deregulated in recurrent tumors thereby indicating that the latter can "normalize" some behaviors to suit their needs. An interactive and freely available software tool was developed to allow continued analyses of these and other transcriptional profiles. Collectively, these studies define the metabolic, biochemical, and molecular events accompanyingHCCevolution, regression, and recurrence in the absence of any potentially confounding therapies.
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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.