ArticleFrontiers in pharmacology2018
SIRT6 Depletion Sensitizes Human Hepatoma Cells to Chemotherapeutics by Downregulating MDR1 Expression.
Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Squalene attenuates doxorubicin resistance in hepatocellular carcinoma by targeting SIRT6 to inhibit ERK1 deacetylation.Molecular and cellular biochemistry · 2026Article
- Emerging Role of Sirtuins-Mediated Ferroptosis in Hepatocellular Carcinoma Progression: Mechanisms and Therapeutic Perspectives.Journal of hepatocellular carcinoma · 2026Review
- L-741626 inhibits hepatocellular carcinoma progression by targeting Ref-1 to suppress MAPK/ERK signalling pathway activity.Biology direct · 2025Article
- The sirtuin family in health and disease.Signal transduction and targeted therapy · 2022Review
- Review
- How Dysregulated Ion Channels and Transporters Take a Hand in Esophageal, Liver, and Colorectal Cancer.Reviews of physiology, biochemistry and pharmacology · 2021Review
- Sirt6 Deacetylase: A Potential Key Regulator in the Prevention of Obesity, Diabetes and Neurodegenerative Disease.Frontiers in pharmacology · 2020Article
- Inhibition of Sirt6 suppresses tumor growth by inducing G1/S phase arrest in renal cancer cells.International journal of clinical and experimental pathology · 2019Article
- SIRT6 Is Involved in the Progression of Ovarian Carcinomas via β-Catenin-Mediated Epithelial to Mesenchymal Transition.Frontiers in oncology · 2018Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multidrug resistance (MDR) due to overexpression of MDR1 is a major obstacle that hinders the treatment of hepatocellular carcinoma (HCC). In this study, we explored the function and underlying molecular mechanism of SIRT6 in MDR of HCC. Chemotherapeutic agents (doxorubicin, cisplatin, and sorafenib) treatment increased SIRT6 mRNA and protein level in two HCC cell lines in a dose-dependent manner. SIRT6 depletion resulted in decreased cell viability and increased apoptosis in HCC cells treated with chemotherapeutic agents. Mechanistically, SIRT6 depletion reduced MDR1 transcription by targeting its promoter in HCC cells treated with chemotherapeutic agents. Consistently, the protein level of MDR1 was also reduced in SIRT6-depleted HCC cells. Further studies indicated that SIRT6 depletion may suppress CCAAT/enhancer binding protein β (C/EBPβ), to act as a transcriptional activator of MDR1 in HCC cells treated with chemotherapeutic agents. Importantly, forced expression of MDR1 could attenuate the apoptosis induced by chemotherapeutic agents in SIRT6-depleted cells. Taken together, these results indicated SIRT6 depletion enhanced chemosensitivity of human hepatoma cells by downregulating MDR1 expression through suppressing C/EBPβ. SIRT6 may serve as a novel target to enhance chemosensitivity in HCC cells.
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