ArticleWorld journal of urology2019
Paclitaxel resistance and the role of miRNAs in prostate cancer cell lines.
Article in World journal of urology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 31 citations in OpenAlex.
- The Managed Acquisition of Chemoresistance as an Informative Tool for Tumor Research.International journal of molecular sciences · 2025Review
- miRNA-mediated resistance mechanisms in prostate cancer: implications for targeted therapy and metastatic progression.Medical oncology (Northwood, London, England) · 2025Review
- Role and potential mechanisms of miR‑100 in different diseases (Review).Oncology reports · 2025Review
- Article
- LncRNAs in modulating cancer cell resistance to paclitaxel (PTX) therapy.Medical oncology (Northwood, London, England) · 2024Review
- Molecular Mechanisms of Prostate Cancer Development in the Precision Medicine Era: A Comprehensive Review.Cancers · 2024Review
- Deregulated microRNAs Involved in Prostate Cancer Aggressiveness and Treatment Resistance Mechanisms.Cancers · 2023Review
- The Profile of MicroRNA Expression and Potential Role in the Regulation of Drug-Resistant Genes in Doxorubicin and Topotecan Resistant Ovarian Cancer Cell Lines.International journal of molecular sciences · 2022Article
- Regulatory functions of miR‑200b‑3p in tumor development (Review).Oncology reports · 2022Review
- Review
- The Profile of MicroRNA Expression and Potential Role in the Regulation of Drug-Resistant Genes in Cisplatin- and Paclitaxel-Resistant Ovarian Cancer Cell Lines.International journal of molecular sciences · 2022Article
- Role of noncoding RNA in drug resistance of prostate cancer.Cell death & disease · 2021Review
- Investigation of the efficacy of paclitaxel on some miRNAs profiles in breast cancer stem cells.Turkish journal of biology = Turk biyoloji dergisi · 2021Article
- LncRNA GAS5 enhances tumor stem cell-like medicated sensitivity of paclitaxel and inhibits epithelial-to-mesenchymal transition by targeting the miR-18a-5p/STK4 pathway in prostate cancer.Asian journal of andrologyArticle
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
purposeTo investigate the expression profiles of 86 miRNAs in paclitaxel-resistant prostate cancer cell lines and to identify the genes that have a role in the development of drug resistance.
methodsThree prostate cancer cell lines, androgen-dependent VCaP, androgen-independent PC-3 and DU-145, were used to obtain paclitaxel-resistant cells by progressively increasing the concentration of paclitaxel in the culture medium. Viability assays with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium and sulforhodamine B were used to assess the cell resistance level and cytotoxic effects of paclitaxel treatment. Total RNA was isolated from both prostate cancer cell lines and their resistant versions, and cDNA samples were reverse transcribed from total RNA. Selected target genes of miRNAs that showed differences in expression and were estimated to be effective on drug resistance mechanism were analyzed with western blot analysis.
resultsExpression study of 86 miRNAs by RT-PCR demonstrated that several of the miRNAs were expressed at different levels in paclitaxel-resistant cells compared to wild-type cells. Moreover, the expression profiles of these miRNAs varied among different prostate cancer cell line types, with 13 miRNAs being up-regulated in the resistant cells. Among these, miR-200b-3p, miR-34b-3p and miR-375 exhibited a marked up-regulation. Further, miR-100-5p showed a prominent increase in paclitaxel-resistant VCaP-R and DU145-R cells. Western blot and RT-PCR studies showed that only the LARP1 and CCND1 genes were over-expressed up to 2-5 times in all paclitaxel-resistant cell lines compared to the other investigated genes.
conclusionsIn this study, the three paclitaxel-resistant prostate cancer cell lines examined showed remarkably different miRNA expression profiles.
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