{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,23]],"date-time":"2026-01-23T20:30:51Z","timestamp":1769200251157,"version":"3.49.0"},"reference-count":35,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2022,5,5]],"date-time":"2022-05-05T00:00:00Z","timestamp":1651708800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Molecular Carcinogenesis"],"published-print":{"date-parts":[[2022,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Diallyl trisulfide (DATS) is a promising small molecule phytochemical that exhibits in vitro and in vivo activity in multiple preclinical solid tumor models including breast cancer, but the underlying mechanism is not fully understood. We have shown previously that forkhead box Q1 (FoxQ1) transcription factor is a novel target for breast cancer stem\u2010like cells (bCSC) inhibition by DATS. Analysis of the breast TCGA (The Cancer Genome Atlas) data revealed that <jats:italic>FoxQ1<\/jats:italic> expression was positively associated with that of <jats:italic>SLC16A1\/monocarboxylate transporter 1<\/jats:italic> (<jats:italic>MCT1)<\/jats:italic>. Western blot analysis confirmed increased expression of MCT1 protein in SUM159 (basal\u2010like) and MCF\u20107 cells (luminal\u2010type) stably transfected to overexpress FoxQ1. Furthermore, FoxQ1 was recruited to the promoter of <jats:italic>SLC16A1<\/jats:italic>\/<jats:italic>MCT1<\/jats:italic>. Treatment of SUM159 and MCF\u20107 cell lines with DATS resulted in suppression of MCT1 protein level that was accompanied by a decrease in intracellular and secreted levels of lactate. Overexpression or knockdown of MCT1 protein failed to alter DATS\u2010mediated inhibition of colony formation or cell migration when compared to corresponding control cells. On the other hand, overexpression of MCT1 protein conferred partial but statistically significant protection against DATS\u2010mediated inhibition of bCSC fraction (CD49f<jats:sup>high<\/jats:sup>\/CD44<jats:sup>high<\/jats:sup> and aldehyde dehydrogenase 1 activity). The size of the mammospheres was relatively smaller in the DATS\u2010treated group compared to control group. Inhibition of bCSC upon DATS treatment was augmented by knockdown of the MCT1 protein. In conclusion, the present study reveals that MCT1 is a novel target for bCSC inhibition by DATS treatment.<\/jats:p>","DOI":"10.1002\/mc.23415","type":"journal-article","created":{"date-parts":[[2022,5,5]],"date-time":"2022-05-05T22:09:35Z","timestamp":1651788575000},"page":"752-763","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Monocarboxylate transporter 1 is a novel target for breast cancer stem like\u2010cell inhibition by diallyl trisulfide"],"prefix":"10.1002","volume":"61","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2071-613X","authenticated-orcid":false,"given":"Su\u2010Hyeong","family":"Kim","sequence":"first","affiliation":[{"name":"Department of Pharmacology &amp; Chemical Biology University of Pittsburgh School of Medicine Pittsburgh Pennsylvania 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