ArticleInternational journal of molecular sciences2025
Sulfatide Acts as a Regulatory Molecule Controlling β1 Integrin-STAT5 Signaling and BOLA2-Dependent Apoptotic Pathway in Breast Cancer Cells.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Dietary Rosmarinic Acid Improved the Growth, Immunity and Antioxidation ofAnimals : an open access journal from MDPI · 2026Article
- UGT8/GalCer-dependent resistance of breast cancer cells to drug-induced apoptosis is potentially regulated by the LIM/homeobox protein LHX6.Scientific reports · 2026Article
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Authors and funding
5 authors.
Funding
Abstract
Cell membrane glycosylations play a critical role in regulating cell signaling, adhesion, and immune recognition. Abnormal glycosylation is a hallmark of cancer and promotes tumor progression. Sulfatide (SM4), a glycosphingolipid synthesized by galactosylceramide sulfotransferase (CST), is frequently altered in cancers, including breast cancer. Our previous studies identified SM4 as an adhesive molecule that enhances metastasis through interactions with platelets and endothelium; however, its elevated levels increase apoptotic sensitivity and reduce tumorigenicity. Here, we elucidate the molecular mechanisms linking sulfatide metabolism to apoptosis and gene regulation. Using MDA-MB-231 and MDA-MB-468 breast cancer cells with altered CST/SM4 levels, RNA sequencing and functional analyses revealed that overproduction of the CST/SM4 significantly downregulated
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