Role of insulin-like growth factor/receptor signaling in hepatocellular carcinoma.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic pathways and literature without systematic search methodology.
PubMed 41589205 · doi:10.14744/hf.2025.11358
What was done
This narrative review summarizes existing literature on the involvement of the insulin-like growth factor (IGF) system—including IGF-1, IGF-2, and their receptors—in the development, progression, and potential therapeutic targeting of hepatocellular carcinoma (HCC).
What was found
The abstract reports no numerical data or statistical effect sizes. It qualitatively reports that HCC is characterized by IGF-1R overexpression, elevated IGF-2 levels, and reduced IGF-1 levels, all associated with poor prognosis. Signaling through IGF-1R activates the PI3K/AKT/mTOR and RAS/RAF/MEK/ERK pathways, driving proliferation and inhibiting apoptosis. Additionally, in diabetes, low IGF-1 levels are associated with increased HCC risk in the setting of hyperinsulinemia, chronic inflammation, non-alcoholic fatty liver disease (NAFLD), and non-alcoholic steatohepatitis (NASH).
Why it matters
It outlines the biological rationale for targeting components of the IGF receptor signaling cascade in hepatocellular carcinoma and links metabolic dysfunction (NAFLD/NASH and diabetes) to hepatic oncogenesis.
Limits
The abstract describes a narrative review rather than a systematic review or meta-analysis. No sample sizes, patient cohorts, quantitative risk estimates, or clinical trial outcomes are reported.
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