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Published on: September 8, 2017
MicroRNA‑302a upregulation mediates chemo‑resistance in prostate cancer cells
Yuqi Wu1, Li Hu1, Zizhen Qin1
1Department of Urology, Carson International Cancer Centre, Shenzhen University General Hospital and Shenzhen University Clinical Medical Academy Centre, Shenzhen University, Shenzhen, Guangdong 518000, P.R. China.
Abstract:
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.
Insights
MicroRNA-302a (miR-302a) upregulation increases paclitaxel resistance in prostate cancer. Inhibiting miR-302a can re-sensitize cancer cells to chemotherapy, offering new therapeutic strategies.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRNAs) are key regulators of gene expression involved in cancer development.
- Altered miRNA expression is linked to chemotherapy resistance in various cancers.
- Prostate cancer often develops resistance to paclitaxel, a common chemotherapeutic agent.
Purpose of the Study:
- To investigate the role of microRNA-302a (miR-302a) in mediating paclitaxel chemoresistance in prostate cancer.
- To determine if miR-302a expression levels correlate with paclitaxel resistance in prostate cancer cells.
Main Methods:
- In vitro analyses using paclitaxel-resistant (PC-3PR) and non-resistant (PC-3) prostate cancer cell lines.
- Assessing miR-302a expression levels in both cell lines.
- Manipulating miR-302a expression (ectopic expression and silencing) to evaluate its effect on paclitaxel sensitivity.
- Analyzing the expression of potential miR-302a target genes, including breast cancer resistance protein (BCRP).
Main Results:
- miR-302a expression was significantly upregulated in paclitaxel-resistant PC-3PR cells compared to PC-3 cells.
- Ectopic expression of miR-302a enhanced paclitaxel resistance in wild-type PC-3 cells.
- Silencing miR-302a in PC-3PR cells sensitized them to paclitaxel.
- The miR-302a target gene BCRP was identified as a potential mediator of paclitaxel resistance.
Conclusions:
- Elevated miR-302a levels contribute to paclitaxel chemoresistance in prostate cancer.
- miR-302a exerts its effect by regulating downstream targets such as AOF2, BCRP, and P-glycoprotein 1.
- Targeting miR-302a may represent a novel therapeutic strategy to overcome paclitaxel resistance in prostate cancer.
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