Radziejewska, K Czerwińska, B Popławska, A Galicka
{"title":"Rosmarinic acid influences the expression of glycoforms in DLD-1 and HT-29 colon cancer cells.","authors":"Radziejewska, K Czerwińska, B Popławska, A Galicka","doi":"10.1016/j.biopha.2025.118432","DOIUrl":null,"url":null,"abstract":"<p><p>Rosmarinic acid (RA) is polyphenolic compound with beneficial, health-promoting effects. Specifically altered glycosylation of cancer cells is strongly related to cancer progress and poor prognosis. Due to limited studies regarding the influence of RA on this process in colon tumor cells, we examined how this acid at concentrations 200 and 400 μM influences selected glycoforms, enzymes taking part in their forming as well as Gal-3 and Akt, in DLD-1 and HT-29 colon cancer cells. To determine the expression of studied factors, RT-qPCR, ELISA and Western blotting were applied. We revealed inhibitory effect of RA in both cell lines on MUC1, ppGalNAcT2, C1GalT1, Cosmc, ST3GalT1, FUT3/4, Gal-3, and Akt mRNAs. ST6GalNAcT1 mRNA was suppressed by both RA concentrations in DLD-1 and by 400 μM RA in HT-29 cell line. In HT-29 cells, both RA concentrations inhibited all examined sugar antigens released to the culture medium and T, sialyl T, and fucosylated epitopes measured in cell lysates. Tn and sialyl Tn antigens in cell lysates were suppressed only by 400 μM RA. In DLD-1 cells, both RA concentrations inhibited sialyl Tn, T antigens in medium and sialyl T in cell lysates. T epitope in lysates was inhibited only by 400 μM RA. Moreover, both RA concentrations suppressed C1GalT1, Gal-3 and pAkt proteins in DLD-1 cells. In HT-29 cells, both RA concentrations suppressed MUC1 extracellular domain; C1GalT1 was diminished by 200 μM RA, Gal-3 and pAkt by 400 μM RA. The data suggest possible benefit of RA as the agent supporting colon cancer treatment.</p>","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":"190 ","pages":"118432"},"PeriodicalIF":7.5000,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1016/j.biopha.2025.118432","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/8/9 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Rosmarinic acid (RA) is polyphenolic compound with beneficial, health-promoting effects. Specifically altered glycosylation of cancer cells is strongly related to cancer progress and poor prognosis. Due to limited studies regarding the influence of RA on this process in colon tumor cells, we examined how this acid at concentrations 200 and 400 μM influences selected glycoforms, enzymes taking part in their forming as well as Gal-3 and Akt, in DLD-1 and HT-29 colon cancer cells. To determine the expression of studied factors, RT-qPCR, ELISA and Western blotting were applied. We revealed inhibitory effect of RA in both cell lines on MUC1, ppGalNAcT2, C1GalT1, Cosmc, ST3GalT1, FUT3/4, Gal-3, and Akt mRNAs. ST6GalNAcT1 mRNA was suppressed by both RA concentrations in DLD-1 and by 400 μM RA in HT-29 cell line. In HT-29 cells, both RA concentrations inhibited all examined sugar antigens released to the culture medium and T, sialyl T, and fucosylated epitopes measured in cell lysates. Tn and sialyl Tn antigens in cell lysates were suppressed only by 400 μM RA. In DLD-1 cells, both RA concentrations inhibited sialyl Tn, T antigens in medium and sialyl T in cell lysates. T epitope in lysates was inhibited only by 400 μM RA. Moreover, both RA concentrations suppressed C1GalT1, Gal-3 and pAkt proteins in DLD-1 cells. In HT-29 cells, both RA concentrations suppressed MUC1 extracellular domain; C1GalT1 was diminished by 200 μM RA, Gal-3 and pAkt by 400 μM RA. The data suggest possible benefit of RA as the agent supporting colon cancer treatment.