MicroRNAs (miRNAs) are post‑transcriptional regulators that mediate the initiation and progression of human cancer. Growing evidence suggests that deregulation of miRNA expression levels underlies chemo‑resistance. To investigate whether miRNA‑302a (miR‑302a) is involved in mediating chemo‑resistance to paclitaxel in prostate cancer, a series of in vitro analyses were performed in paclitaxel‑resistant prostate cancer PC‑3PR cells and non‑resistant prostate cancer PC‑3 cells. It was demonstrated that the expression of miR‑302a was upregulated in PC‑3PR cells. Notably, ectopic expression of miR‑302a also increased resistance to paclitaxel in wild‑type PC‑3 cells. By contrast, silencing of miR‑302a in PC‑3PR cells sensitized the cells to paclitaxel. Gene and protein expression analyses suggested that the miR‑302a target gene breast cancer resistance protein (BCRP) may mediate chemo‑resistance to paclitaxel in PC‑3PR cells. In conclusion, the data suggested that elevated miR‑302a levels, in part, mediate sensitivity to paclitaxel in prostate cancer through the aberrant regulation of its downstream targets, AOF2, BCRP and permeability glycoprotein 1. These data have implications for the development of novel therapeutics in prostate cancer that may improve sensitivity to chemotherapeutics.
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http://dx.doi.org/10.3892/mmr.2019.10098 | DOI Listing |
EClinicalMedicine
February 2025
Blavatnik Faculty Fellow in Health and Longevity, Beth Israel Deaconess Medical Center, Harvard Medical School, USA.
Front Immunol
January 2025
Division of Urology, Department of Surgery, Endeavor Health (formerly NorthShore University HealthSystem), Evanston, IL, United States.
Introduction: Macrophages exhibit marked phenotypic heterogeneity within and across disease states, with lipid metabolic reprogramming contributing to macrophage activation and heterogeneity. Chronic inflammation has been observed in human benign prostatic hyperplasia (BPH) tissues, however macrophage activation states and their contributions to this hyperplastic disease have not been defined. We postulated that a shift in macrophage phenotypes with increasing prostate size could involve metabolic alterations resulting in prostatic epithelial or stromal hyperplasia.
View Article and Find Full Text PDFFront Immunol
January 2025
Department of Urology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen, China.
Prostate-Specific Membrane Antigen (PSMA) is a highly expressed and structurally unique target specific to prostate cancer (PCa). Diagnostic and therapeutic approaches in nuclear medicine, coupling PSMA ligands with radionuclides, have shown significant clinical success. PSMA-PET/CT effectively identifies tumors and metastatic lymph nodes for imaging purposes, while -PSMA-617 (Pluvicto) has received FDA approval for treating metastatic castration-resistant PCa (mCRPC).
View Article and Find Full Text PDFClin Transl Radiat Oncol
March 2025
University Medical Center Utrecht, Department of Radiation Oncology, Utrecht, the Netherlands.
Background And Purpose: This study assessed the treatment time of online adaptive (i.e. Adapt-to-Shape, ATS) and virtual couch shift (i.
View Article and Find Full Text PDFBackground And Aims: Even though aging is a known risk factor for prostate cancer incidence and mortality, there has been an increase in incidence among young men since the late 1980s with notably lower survival rates than those among older men. However, there is insufficient knowledge about recent trends in the incidence and survival of this disease.
Methods: We analyzed prostatic cancer incidence trends in men under 50 from 1975 to 2020 using Surveillance, Epidemiology, and End Results (SEER) 8 registries data.
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