ArticleAutophagy reports2024
Simultaneous activation and blockade of autophagy to fight hepatocellular carcinoma.
Article in Autophagy reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Simultaneous activation and late-stage inhibition of autophagy induces autophagy-dependent cell death in leukemia.BMC cancer · 2026Article
- Lysosome-dependent cell death in hepatocellular carcinoma: unlocking the therapeutic potential of natural products.Frontiers in pharmacology · 2026Review
- Selective autophagy in hepatocellular carcinoma: Mechanisms, roles and therapeutic implications (Review).Experimental and therapeutic medicine · 2025Review
- Review
- Anti-Cancer Strategy Based on Changes in the Role of Autophagy Depending on the Survival Environment and Tumorigenesis Stages.Molecules (Basel, Switzerland) · 2024Review
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Authors and funding
7 authors.
Funding
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Abstract
Autophagy is considered a target for cancer treatment, although few compounds manipulating this process have been added to the anticancer arsenal in humans. Pharmacological manipulation of autophagy has therefore been considered in the treatment and chemosensitization of hepatocellular carcinoma (HCC), a heterogeneous malignancy that remains difficult to treat (limited impact of genomic discoveries for the implementation of personalized precision medicine). We analyzed the autophagy marker proteins p62 and LC3 in paired tumor and adjacent cirrhotic non-tumor tissues of human HCC. We show strong variability in p62 and LC3-II levels between tumor parts of different HCC patients and between tumor and non-tumor HCC in the same patient, suggesting heterogeneity in autophagy flux. This diversity in flux led us to consider a non-personalized method of autophagy targeting, combining simultaneous activation and blockade of autophagy, which could, in theory, benefit a substantial number of HCC patients, irrespective of tumor autophagic flux. We show that the combination of sodium butyrate (NaB, autophagy inducer) and chloroquine (CQ, autophagy blocker) has a marked and synergistic cytotoxic effect in vitro on all human liver cancer cell lines studied, compared with the cellular effect of each product separately, and with no deleterious effect on normal hepatocytes in culture. Cancer cell death was associated with accumulation of autophagosomes, induction of lysosome membrane permeabilization and increased oxidative stress. Our results suggest that simultaneous activation and blockade of autophagy may be a valuable approach against HCC, and that microbiota-derived products improve the sensitivity of HCC cells to antitumor agents.
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