A metabolic switch enables hepatocytes in damaged livers to escape senescence and form tumors.
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Bypassing senescence.
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January 2025
Science Signaling, AAAS, Washington, DC 20005, USA. Email:
A metabolic switch enables hepatocytes in damaged livers to escape senescence and form tumors.
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Glioblastoma (GBM) characterized byits rapid progression and challenging prognosis, often featuring mutations in the Kirsten rat sarcoma virus (KRAS) gene, which is crucial for numerous cellular signaling mechanisms. Emerging research underscores a significant interaction between KRAS and microRNAs (miRNAs) in these cancers, with miRNAs playing key roles as both regulators and mediators within the KRAS signaling framework. The concept of oncogene-induced senescence (OIS) is explored as a protective mechanism against tumor development, examining how K-RAS signaling is meticulously adjusted to bypass senescence, thereby enhancing cell growth and survival.
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Laboratory of Gene Regulation and Signal Transduction, Departments of Pharmacology and Pathology, School of Medicine, University of California San Diego (UCSD), La Jolla, CA, USA.
Article Synopsis
- Hepatocellular carcinoma (HCC) arises from liver cells (hepatocytes) that are damaged and undergoing compensatory growth, particularly due to metabolic disorders like MASH.
- The tumor-suppressive effects of p53 and the anti-cancer role of the enzyme FBP1 are undermined in HCC, as FBP1 is commonly degraded and suppressed in tumors.
- Key metabolic pathways involving AKT and NRF2 play a role in reversing the effects of cellular senescence, boosting the growth of HCC cells and leading to the accumulation of genetic mutations that contribute to cancer progression.
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