ArticleThe Journal of biological chemistry2017
The Glycosyltransferase ST6Gal-I Protects Tumor Cells against Serum Growth Factor Withdrawal by Enhancing Survival Signaling and Proliferative Potential.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 48 citations in OpenAlex.
- Development of a Novel, Potent, and Selective Sialyltransferase Inhibitor for Suppressing Cancer Metastasis.International journal of molecular sciences · 2024Article
- Role of ST6GAL1 and ST6GAL2 in subversion of cellular signaling during enteroaggregative Escherichia coli infection of human intestinal epithelial cell lines.Applied microbiology and biotechnology · 2023Article
- Role of tumor cell sialylation in pancreatic cancer progression.Advances in cancer research · 2023Review
- Role of a Disease-associated ST3Gal-4 in Non-small Cell Lung Cancer.Cell biochemistry and biophysics · 2022Article
- Sialyltransferases and Neuraminidases: Potential Targets for Cancer Treatment.Diseases (Basel, Switzerland) · 2022Review
- α2,6 Sialylation mediated by ST6GAL1 promotes glioblastoma growth.JCI insight · 2022Article
- The incorrect use of CD75 as a synonym for ST6GAL1 has fostered the expansion of commercial "ST6GAL1" antibodies that do not recognize ST6GAL1.Glycobiology · 2022Article
- Altered glycosylation in pancreatic cancer and beyond.The Journal of experimental medicine · 2022Review
- Bacterial colonization and TH17 immunity are shaped by intestinal sialylation in neonatal mice.Glycobiology · 2022Article
- ST6Gal1: Oncogenic signaling pathways and targets.Frontiers in molecular biosciences · 2022Review
- Ninety-six-hour starved peripheral blood mononuclear cell supernatant inhibited LA7 breast cancer stem cells induced tumorFrontiers in immunology · 2022Article
- Terminal α2,6-sialylation of epidermal growth factor receptor modulates antibody therapy response of colorectal cancer cells.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- Regulation of ST6GAL1 sialyltransferase expression in cancer cells.Glycobiology · 2021Review
- Association of ST6GAL1 and CYP19A1 polymorphisms in the 3'-UTR with astrocytoma risk and prognosis in a Chinese Han population.BMC cancer · 2021Article
- Downregulation of Stemness Genes and Induction of Necrosis in Rat LA7 Cancer Stem Cells Induced Tumors Treated with Starved Fibroblasts Culture Supernatant.Reports of biochemistry & molecular biology · 2021Article
- Heterogeneity in 2,6-Linked Sialic Acids Potentiates Invasion of Breast Cancer Epithelia.ACS central science · 2021Article
- Sialylation of FGFR1 by ST6Gal‑I overexpression contributes to ovarian cancer cell migration and chemoresistance.Molecular medicine reports · 2020Article
- Systemic effects of starved fibroblast culture supernatant on immunosuppressed rats treated with cancer stem cells (LA7).Caspian journal of internal medicine · 2020Article
- B cells suppress medullary granulopoiesis by an extracellular glycosylation-dependent mechanism.eLife · 2019Article
- I-branched carbohydrates as emerging effectors of malignant progression.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
A hallmark of cancer cells is the ability to survive and proliferate when challenged with stressors such as growth factor insufficiency. In this study, we report a novel glycosylation-dependent mechanism that protects tumor cells from serum growth factor withdrawal. Our results suggest that the β-galactoside α-2,6-sialyltransferase 1 (ST6Gal-I) sialyltransferase, which is up-regulated in numerous cancers, promotes the survival of serum-starved cells. Using ovarian and pancreatic cancer cell models with ST6Gal-I overexpression or knockdown, we find that serum-starved cells with high ST6Gal-I levels exhibit increased activation of prosurvival signaling molecules, including pAkt, p-p70S6K, and pNFκB. Correspondingly, ST6Gal-I activity augments the expression of tumor-promoting pNFκB transcriptional targets such as IL-6, IL-8, and the apoptosis inhibitor cIAP2. ST6Gal-I also potentiates expression of the cell cycle regulator cyclin D2, leading to increased phosphorylation and inactivation of the cell cycle inhibitor pRb. Consistent with these results, serum-starved cells with high ST6Gal-I expression maintain a greater number of S phase cells compared with low ST6Gal-I expressors, reflecting enhanced proliferation. Finally, selective enrichment in clonal variants with high ST6Gal-I expression is observed upon prolonged serum deprivation, supporting the concept that ST6Gal-I confers a survival advantage. Collectively, these results implicate a functional role for ST6Gal-I in fostering tumor cell survival within the serum-depleted tumor microenvironment.
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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 Socratic graph.