ArticleCancer science2022
SHARPIN promotes cell proliferation of cholangiocarcinoma and inhibits ferroptosis via p53/SLC7A11/GPX4 signaling.
Article in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 2 of them syntheses that pooled it.
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Who cites it
76 citing papers in PubMed, 2 syntheses or guidelines pooled it, 118 citations in OpenAlex.
- The interaction between endoplasmic reticulum stress and ferroptosis in ovarian diseases.Journal of ovarian research · 2026Pooled it
- Global research trends and frontiers in ferroptosis in hepatocellular carcinoma: a bibliometric and visualization study.Frontiers in oncology · 2024Pooled it
- miR-29a-3p regulates SPARC to inhibit ferroptosis and promote cell proliferation in gastric cancer.Scientific reports · 2026Article
- Experimental Validation of an Immune Cell Infiltration Signature in Psoriasis: Translating Computational Modeling to In Vivo Efficacy.Journal of clinical laboratory analysis · 2026Article
- Pseudolaric acid B promotes lung cancer cells ferroptosis depending on JNK/ERK-mediated upregulation of survivin.Scientific reports · 2026Article
- Fucoxanthin Induces Ferroptosis in Hypopharyngeal Carcinoma Cells by Activating the p53/SLC7A11/GPX4 Axis.Marine drugs · 2026Article
- Post-translational modifications in ferroptosis: mechanisms and therapeutic potential.International journal of biological sciences · 2026Review
- Ferroptosis in biliary tract cancer: Molecular mechanisms and therapeutic applications (Review).International journal of oncology · 2026Review
- Traumatic brain injury-related ferroptosis: current perspectives.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Characterization of Differential GPX4 Essentiality Between Intrahepatic and Extrahepatic Cholangiocarcinoma via Leveraging of a Large-Scale Functional Genomic Screen.International journal of molecular sciences · 2025Article
- Potential Mechanisms of Exercise-Mediated Ferroptosis Regulation in Central Nervous System Diseases.Molecular neurobiology · 2025Review
- Ferroptosis: molecular mechanisms, pathophysiology, and role in pediatric pulmonary diseases.Cell biology and toxicology · 2025Review
- New evidence for the protective effect of gut microbiota regulation of ferroptosis-related proteins against osteoporosis.World journal of microbiology & biotechnology · 2025Article
- Zingerone treats postmenopausal osteoporosis via increased ferroptosis sensitivity by p53-mediated regulation of SAT1 and GPX4 expression.Communications biology · 2025Article
- METTL3/YTHDF3 mJournal of diabetes investigation · 2025Article
- YY1-induced USP43 drives ferroptosis suppression by FASN stabilization and subsequent activation of SLC7A11 in ovarian cancer.Cell death & disease · 2025Article
- Intersection of ferroptosis and nanomaterials brings benefits to breast cancer.Cell biology and toxicology · 2025Review
- Ferroptosis in cancer: revealing the multifaceted functions of mitochondria.Cellular and molecular life sciences : CMLS · 2025Review
- Modified Qianghuo Shengshi Decoction Ameliorates Osteoarthritis via Inhibiting PI3K/Akt Pathway-Related Ferroptosis.Journal of cellular and molecular medicine · 2025Article
- Inhibition of histone deacetylases 3 attenuates imiquimod-induced psoriatic dermatitis via targeting cGAS-STING signaling in keratinocytes.Journal of translational medicine · 2025Article
16 more citing papers are in PubMed but not listed here.
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12 authors at 1 institution in 1 country.
Funding
Abstract
SHARPIN is a tumor-associated gene involved in the growth and proliferation of many tumor types. A function of SHARPIN in cholangiocarcinoma (CCA) is so far unclear. Here, we studied the role and function of SHARPIN in CCA and revealed its relevant molecular mechanism. The expression of SHARPIN was analyzed in cholangiocarcinoma tissues from patients using immunohistochemistry, quantitative PCR, and western blot analysis. Expression of SHARPIN was suppressed/overexpressed by siRNA silencing or lentiviral overexpression vector, and the effect on cell proliferation was determined by the CCK-8 assay and flow cytometry. Accumulation of reactive oxygen species was measured with MitoTracker, and JC-1 staining showed mitochondrial fission/fusion and mitochondrial membrane potential changes as a result of the silencing or overexpression. The ferroptosis marker solute carrier family 7 member 11 (SLC7A11), glutathione peroxidase 4 (GPX4), and the antioxidant enzymes superoxide dismutase 1 (SOD-1) and SOD-2 were analyzed by western blot. The results showed that SHARPIN expression was increased in CCA tissue, and this was involved in cell proliferation. SHARPIN silencing resulted in accumulated reactive oxygen species, reduced mitochondrial fission, and a reduced mitochondrial membrane potential. Silencing of SHARPIN inhibited the ubiquitination and degradation of p53, and downregulated levels of SLC7A11, GPX4, SOD-1, and SOD-2, all of which contributed to excessive oxidative stress that leads to ferroptosis. Overexpression of SHARPIN would reverse the above process. The collected data suggest that in CCA, SHARPIN-mediated cell ferroptosis via the p53/SLC7A11/GPX4 signaling pathway is inhibited. Targeting SHARPIN might be a promising approach for the treatment of CCA.
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