ArticleMolecular and cellular biochemistry2016
GalNAc-T4 putatively modulates the estrogen regulatory network through FOXA1 glycosylation in human breast cancer cells.
Article in Molecular and cellular biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 28 citations in OpenAlex.
- TRIM23 promotes 5-Fluorouracil resistance in colorectal cancer by upregulating GALNT4 expression.Apoptosis : an international journal on programmed cell death · 2025Article
- BarH-Like Homeobox 2 Suppresses Cell Proliferation, Invasion, and Angiogenesis in Hepatocellular Carcinoma by Activating N-Acetylgalactosaminyltransferase 4.Molecular biotechnology · 2024Article
- The expression of O-linked glycosyltransferase GALNT7 in breast cancer is dependent on estrogen-, progesterone-, and HER2-receptor status, with prognostic implications.Glycoconjugate journal · 2023Article
- Unconventional protein post-translational modifications: the helmsmen in breast cancer.Cell & bioscience · 2022Review
- Altered glucuronidation deregulates androgen dependent response profiles and signifies castration resistance in prostate cancer.Oncotarget · 2021Article
- Mucins as anti-cancer targets: perspectives of the glycobiologist.Glycoconjugate journal · 2021Review
- Ser and Thr acceptor preferences of the GalNAc-Ts vary among isoenzymes to modulate mucin-type O-glycosylation.Glycobiology · 2020Article
- miR-365b regulates the development of non-small cell lung cancer via GALNT4.Experimental and therapeutic medicine · 2020Article
- Identification of Tn antigen O-GalNAc-expressing glycoproteins in human carcinomas using novel anti-Tn recombinant antibodies.Glycobiology · 2020Article
- MiR-4262 promotes cell apoptosis and inhibits proliferation of colon cancer cells: involvement of GALNT4.American journal of translational research · 2018Article
- miR‑4262 inhibits colon cancer cell proliferation via targeting of GALNT4.Molecular medicine reports · 2017Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
GALNT4 belongs to a family of N-acetylgalactosaminyltransferases, which catalyze the transfer of GalNAc to Serine or Threonine residues in the initial step of mucin-type O-linked protein glycosylation. This glycosylation type is the most complex post-translational modification of proteins, playing important roles during cellular differentiation and in pathological disorders. Most of the breast cancer subtypes are estrogen receptor positive, and hence, the estrogen pathway represents a key regulatory network. We investigated the expression of GalNAc-T4 in a panel of mammary epithelial cell lines and found its expression is associated with the estrogen status of the cells. FOXA1, a key transcription factor, functions to promote estrogen responsive gene expression by acting as a cofactor to estrogen receptor alpha (ERα), but all the aspects of this regulatory mechanism are not fully explored. This study found that knockdown of GALNT4 expression in human breast cancer cells attenuated the protein expression of ERα, FOXA1, and Cyclin D1. Further, our immunoprecipitation assays depicted the possibility of FOXA1 to undergo O-GalNAc modifications with a decrease of GalNAc residues in the GALNT4 knockdown cells and also impairment in the FOXA1-ERα association. Rescuing GALNT4 expression could restore the interaction as well as the glycosylation of FOXA1. Together, these findings suggest a key role for GalNAc-T4 in the estrogen pathway through FOXA1 glycosylation.
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