Ertürk, ElifArı, FerdaAkgün, OguzhanUlukaya, EnginKüçükali, Cem İsmailZeybek, Ümit2024-06-112024-06-112021-01-011300-0152https://doi.org/10.3906/biy-2103-46https://journals.tubitak.gov.tr/biology/vol45/iss5/3/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8574192/https://hdl.handle.net/11452/41982Understanding of the functions of microRNAs in breast cancer and breast cancer stem cells have been a hope for the development of new molecular targeted therapies. Here, it is aimed to investigate the differences in the expression levels of let-7a, miR-10b, miR-21, miR-125b, miR-145, miR-155, miR-200c, miR-221, miR-222 and miR-335, which associated with gene and proteins in MCF-7 (parental) and MCF-7s (Mammosphere/stem cell-enriched population/CD44+/CD24-cells) cells treated with paclitaxel. MCF7-s were obtained from parental MCF-7 cells. Cytotoxic activity of paclitaxel was determined by ATP assay. Total RNA isolation and cDNA conversion were performed from the samples. Changes in expression levels of miRNAs were examined by RT-qPCR. Identified target genes and proteins of miRNAs were analyzed with RT-qPCR and western blot analysis, respectively. miR-125b was significantly expressed (2.0946-fold; p = 0.021) in MCF-7s cells compared to control after treatment with paclitaxel. Downregulation of SMO, STAT3, NANOG, OCT4, SOX2, ERBB2 and ERBB3 and upregulation of TP53 genes were significant after 48 h treatment in MCF-7s cells. Protein expressions of SOX2, OCT4, SMAD4, SOX2 and OCT4 also decreased. Paclitaxel induces miR-125b expression in MCF-7s cells. Upregulation of miR-125b may be used as a biomarker for the prediction of response to paclitaxel treatment in breast cancer.eninfo:eu-repo/semantics/openAccessAtp assayResistanceMicrornasPrognosisBiomarkersCisplatinDiagnosisMir-125bTargetsTumorsBreast cancerStem cellsMcf-7sMir-125bPaclitaxelScience & technologyLife sciences & biomedicineBiologyInvestigation of the efficacy of paclitaxel on some miRNAs profiles in breast cancer stem cellsArticle000708974500003613+45510.3906/biy-2103-461303-6092