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• W2783012254 abstract "Docetaxel (DTX)-based chemotherapy is a first-line therapy in patients with castration-resistant prostate cancer. However, development of DTX resistance remains a challenge in cancer treatment. miRNAs have been shown to be involved in drug resistance in tumors. Nevertheless, little is known about the function and detailed molecular mechanism of miR-133b in DTX resistance of prostate cancer cells. The current study showed that miR-133b was downregulated, while human antigen R (HuR) was upregulated in prostate cancer cells. HuR was identified as a target of miR-133b, and miR-133b could suppress HuR expression. Ectopic expression of miR-133b and HuR knockdown suppressed cell viability and promoted DTX-induced apoptosis in DTX-treated prostate cancer cells, which were restored by HuR overexpression. Furthermore, HuR overexpression partially abolished the inhibitory effect of miR-133b overexpression on ATP-binding cassette (ABC) subfamily G member 2 (ABCG2) expression in prostate cancer cells. ABCG2 overexpression relieved DTX and miR-133b cytotoxicity in prostate cancer cells. In conclusion, posttranscriptional regulation of HuR by miR-133b enhances DTX cytotoxicity through inhibition of ABCG2, revealing a novel miR-133b/HuR/ABCG2 regulatory pathway to overcome chemoresistance in prostate cancer cells." @default.
• W2783012254 created "2018-01-26" @default.
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• W2783012254 date "2018-03-01" @default.
• W2783012254 modified "2023-10-16" @default.
• W2783012254 title "Posttranscriptional Regulation of Human Antigen R by miR-133b Enhances Docetaxel Cytotoxicity Through the Inhibition of ATP-Binding Cassette Subfamily G Member 2 in Prostate Cancer Cells" @default.
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• W2783012254 doi "https://doi.org/10.1089/dna.2017.3940" @default.
• W2783012254 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29327946" @default.
• W2783012254 hasPublicationYear "2018" @default.
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