ArticleJournal of ovarian research2013
ST6Gal-I sialyltransferase confers cisplatin resistance in ovarian tumor cells.
Article in Journal of ovarian research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 112 citations in OpenAlex.
- Aberrant sialylation in cancer: From molecular mechanisms to potential therapeutics.Genes & diseases · 2026Review
- Gamma-irradiated Newcastle disease virus: an alternative inactivated oncolytic virotherapy.Immunology and cell biology · 2026Article
- Writers and readers of sialylation in immunoregulation in cancer.The Journal of biological chemistry · 2026Review
- Aberrant Sialylation in Ovarian Cancer: Orchestrating Progression, Metastasis, and Therapeutic Hurdles.Current medical science · 2025Review
- Sialylation Inhibition Can Partially Revert Acquired Resistance to Enzalutamide in Prostate Cancer Cells.Cancers · 2024Article
- Sialic acid in the regulation of blood cell production, differentiation and turnover.Immunology · 2024Review
- Novel players in the development of chemoresistance in ovarian cancer: ovarian cancer stem cells, non-coding RNA and nuclear receptors.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- Cell Membrane Sialome: Sialic Acids as Therapeutic Targets and Regulators of Drug Resistance in Human Cancer Management.Cancers · 2023Review
- Role of the ST6GAL1 sialyltransferase in regulating ovarian cancer cell metabolism.Glycobiology · 2023Article
- Article
- Role of tumor cell sialylation in pancreatic cancer progression.Advances in cancer research · 2023Review
- Intact glycopeptides identified by LC-MS/MS as biomarkers for response to chemotherapy of locally advanced cervical cancer.Frontiers in oncology · 2023Article
- Sialyltransferases and Neuraminidases: Potential Targets for Cancer Treatment.Diseases (Basel, Switzerland) · 2022Review
- Insights into the Role of Sialylation in Cancer Metastasis, Immunity, and Therapeutic Opportunity.Cancers · 2022Review
- α2,6 Sialylation mediated by ST6GAL1 promotes glioblastoma growth.JCI insight · 2022Article
- Genetic variation in ST6GAL1 is a determinant of capecitabine and oxaliplatin induced hand-foot syndrome.International journal of cancer · 2022Article
- Review
- Unique Glycoform-Dependent Monoclonal Antibodies for Mouse Mucin 21.International journal of molecular sciences · 2022Article
- Identification of α1,2-fucosylated signaling and adhesion molecules in head and neck squamous cell carcinoma.Glycobiology · 2022Article
- In SituCancers · 2022Article
9 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPlatinum drugs, including cisplatin, are a frontline therapeutic in ovarian cancer treatment and acquired resistance to these agents is a major contributor to ovarian cancer morbidity and mortality. In this study a novel glycosylation-dependent mechanism for cisplatin resistance is described. Specifically, cisplatin-induced cell death is blocked by the activity of the ST6Gal-I sialyltransferase. ST6Gal-I modifies specific receptors by adding a negatively charged sialic acid sugar which influences diverse receptor functions. Overexpression of ST6Gal-I is a hallmark of ovarian and other cancers and its expression has been correlated to metastasis and poor prognosis.
methodsTumor cell viability and apoptotic induction were determined in cell lines with ST6Gal-I overexpression and knockdown. In addition, cell populations with acquired resistance to cisplatin were assayed for endogenous ST6Gal-I expression.
resultsWe show that forced expression of ST6Gal-I in OV4 ovarian cancer cells that lack endogenous ST6Gal-I causes reduced activation of caspase 3 and increased cell viability following cisplatin treatment. Conversely, forced ST6Gal-I knockdown in Pa-1 cells with high endogenous ST6Gal-I increases cisplatin-induced caspase activation and cell death. A2780 ovarian cancer cells selected for stable cisplatin resistance display upregulated endogenous ST6Gal-I when compared with parental, cisplatin-sensitive, A2780 cells. Similarly, extended low dose cisplatin treatment of a Pa-1 polyclonal ST6Gal-I shRNA knockdown population led to selection for subclones with elevated ST6Gal-I expression.
conclusionsReceptor sialylation by ST6Gal-I confers a survival advantage for tumor cells in the presence of cisplatin. These collective findings support a role for ST6Gal-I in chemoresistance and highlight ST6Gal-I as a potential therapeutic target for platinum resistant tumors.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.