ArticleCell death & disease2018
Nuclear galectin-1-FOXP3 interaction dampens the tumor-suppressive properties of FOXP3 in breast cancer.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- FKH domain-mediated nuclear FOXP3 suppresses gastric cancer malignancy via c-MYC/CDKN1A regulation, EMT inhibition, and PI3K/AKT signaling modulation.Molecular and cellular biochemistry · 2026Article
- The role of glycan-lectin interactions in the tumor microenvironment: immunosuppression regulators of colorectal cancer.American journal of cancer research · 2025Review
- Galectins in epithelial-mesenchymal transition: roles and mechanisms contributing to tissue repair, fibrosis and cancer metastasis.Biological research · 2024Review
- Advances in Foxp3+ regulatory T cells (Foxp3+ Treg) and key factors in digestive malignancies.Frontiers in immunology · 2024Review
- Generation and characterization of a monoclonal antibody that binds to Galectin-1.Protein expression and purification · 2023Article
- Endogenous Galectin-1 Modulates Cell Biological Properties of Immortalized Retinal Pigment Epithelial Cells In Vitro.International journal of molecular sciences · 2023Article
- Article
- Galectins as pivotal components in oncogenesis and immune exclusion in human malignancies.Frontiers in immunology · 2023Review
- Galectin‑1 binds GRP78 to promote the proliferation and metastasis of gastric cancer.International journal of oncology · 2022Article
- Article
- Inhibition of galectins in cancer: Biological challenges for their clinical application.Frontiers in immunology · 2022Review
- Tanshinone IIA regulates microRNA‑125b/foxp3/caspase‑1 signaling and inhibits cell viability of nasopharyngeal carcinoma.Molecular medicine reports · 2021Article
- Forkhead box P3 promotes breast cancer cell apoptosis by regulating programmed cell death 4 expression.Oncology letters · 2020Article
- FOXP3 promotes colorectal carcinoma liver metastases by evaluating MMP9 expression via regulating S-adenosylmethionine metabolism.Annals of translational medicine · 2020Article
- Nuclear FAM289-Galectin-1 interaction controls FAM289-mediated tumor promotion in malignant glioma.Journal of experimental & clinical cancer research : CR · 2019Article
- miR-664a-3p functions as an oncogene by targeting Hippo pathway in the development of gastric cancer.Cell proliferation · 2019Article
- CD8American journal of translational research · 2019Article
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Authors and funding
17 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FOXP3 is an important X-linked suppressor of breast cancer. It is reported that FOXP3 is usually mutant, absent, or cytoplasmic distribution in breast cancer cells, which increases the risk of breast cancer. However, in our study the full-length FOXP3 transcript can be detected in breast cancer cells and nuclear FOXP3 is expressed in some breast cancer samples. Therefore, an important question is how the tumor-suppressive function of wild-type FOXP3 is negated in these cancers. We found that Gal-1 is a novel interacting protein of FOXP3 in breast cancer. Furthermore, our results show that the FKH domain in FOXP3 is essential for its interaction with Gal-1. Through ChIP-seq assay, we found that the expression of Gal-1 could inhibit a variety of target genes which were directly regulated by FOXP3. More importantly, these FOXP3-bound genes are involved in the development and metastasis of cancer. Furthermore, functional studies revealed that blocking the FOXP3/Gal-1 interaction restores the tumor-suppressive properties of FOXP3 in breast cancer cells. Finally, we observed that the nuclear abundance of Gal-1 was significantly higher in breast cancer tissues than that in adjacent normal tissues. In addition, we identified that the acidic extracellular microenvironment in breast cancer tissues causes Gal-1 to accumulate in the nucleus. Altogether, nuclear Gal-1 interferes with the binding of FOXP3 to DNA by interacting with the FKH domain of FOXP3, and it indicates a possible mechanism for the loss of the tumor-suppressive properties of FOXP3 in wild-type FOXP3-positive breast cancer.
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