Key result
CD36 inhibition resensitizes resistant HCC cells to TKIs by blocking CD276-mediated lipid metabolism reprogramming.
Why the study?
Tyrosine kinase inhibitor-based systemic therapy in advanced hepatocellular carcinoma is frequently limited by drug resistance, the mechanisms of which remain incompletely understood.
The CD276-pSTAT3-CD36 axis drives TKI resistance in HCC via lipid metabolic reprogramming, and targeting CD36 may overcome this resistance.
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CD276 inhibition merits testing to restore TKI sensitivity in HCC; leaves open clinical efficacy pending validation.
Huang et al. (2026) studied advanced hepatocellular carcinoma (HCC). Pharmacological inhibition of CD36 with sulfosuccinimidyl oleate sodium was evaluated on TKI resistance and lipid metabolism. CD276 promotes TKI resistance in HCC by reprogramming lipid metabolism via the pSTAT3-CD36 axis, and pharmacological inhibition of CD36 resensitizes resistant HCC cells to TKIs.
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