ArticleMedical science monitor : international medical journal of experimental and clinical research2018
The Sineoculis Homeobox Homolog 1 (SIX1) Gene Regulates Paclitaxel Resistance by Affecting Reactive Oxygen Species and Autophagy in Human Hepatocellular Carcinoma Cell Line HepG2.
Article in Medical science monitor : international medical journal of experimental and clinical research, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Developing Potent Therapeutics for Liver Cancer Chemoresistance via an RNA Nanotech and Series-Circuit-Christmas-Bulb Mechanism Targeting ABC Transporters.Molecular pharmaceutics · 2026Review
- Sine oculis homeobox homolog family function in gastrointestinal cancer: Progression and comprehensive analysis.World journal of clinical oncology · 2025Review
- Article
- High expression of SIX1 is an independent predictor of poor prognosis in endometrial cancer.American journal of translational research · 2021Article
- Analysis of Key Genes Regulating the Warburg Effect in Patients with Gastrointestinal Cancers and Selective Inhibition of This Metabolic Pathway in Liver Cancer Cells.OncoTargets and therapy · 2020Article
- Achillin Increases Chemosensitivity to Paclitaxel, Overcoming Resistance and Enhancing Apoptosis in Human Hepatocellular Carcinoma Cell Line Resistant to Paclitaxel (Hep3B/PTX).Pharmaceutics · 2019Article
- Antitumor effects of arsenic disulfide on the viability, migratory ability, apoptosis and autophagy of breast cancer cells.Oncology reports · 2019Article
- Lin28b is involved in curcumin-reversed paclitaxel chemoresistance and associated with poor prognosis in hepatocellular carcinoma.Journal of Cancer · 2019Article
- lncRNAOncoTargets and therapy · 2019Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND The objective of this study was to explore the role of SIX1 in paclitaxel (TAX) resistance of HepG2 cells via reactive oxygen species (ROS) and autophagy pathway. MATERIAL AND METHODS Hepatoma cell line HepG2 was treated with SIX1 knockdown or/and TAX. Cell growth was detected by MTT assay and colony formation assay. Cell apoptosis was evaluated with flow cytometry. ROS levels were detected using flow cytometry (stained with DCFH2-DA). Western blot was conducted to detect the expression of SIX1 and autophagy-related proteins. RESULTS TAX suppressed the proliferation of HepG2 cells in a time/dose-dependent manner, and upregulated the expression of SIX1. SIX1 siRNA increased TAX sensitivity of HepG2 cells and upregulated cell ROS levels. SIX1 siRNA combined with TAX treatment activated autophagy of HepG2 cells. N-acetyl-L-cysteine (NAC) partially attenuated SIX1 siRNA-induced ROS level increases, and autophagy inhibitor 3-MA notably enhanced SIX1 siRNA-induced cell apoptosis. CONCLUSIONS Knockdown of SIX1 increased cell ROS levels and autophagy, promoted cell apoptosis, and enhanced TAX sensitivity of HepG2 cells.
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Registered trials
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