β,β-Dimethylacrylshikonin suppresses hepatocellular carcinoma progression through mitochondrial stress and TGM2-associated mitophagy impairment - PubMed
3 hours ago
- #TGM2
- #Hepatocellular Carcinoma
- #Mitophagy
- DMAS, a naphthoquinone derivative, inhibits hepatocellular carcinoma (HCC) cell proliferation and migration by inducing mitochondrial-dependent apoptosis and blocking epithelial-mesenchymal transition (EMT).
- DMAS induces mitochondrial dysfunction and activates PINK1/Parkin signaling to initiate mitophagy, but simultaneously inhibits TGM2, impairing autophagosome formation and leading to accumulation of damaged mitochondria.
- The study shows that DMAS directly binds to TGM2, suppressing Beclin1 and ATG5 expression, which hinders effective mitophagy and enhances antitumor effects in HCC.
- DMAS demonstrates synergistic effects with lenvatinib in suppressing HCC progression, offering a potential new therapeutic strategy for the disease.