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Updated: Jan 7, 2026

MicroRNA Detection in Prostate Tumors by Quantitative Real-time PCR qPCR
Published on: May 16, 2012
Curcumin targets miR-21-3p: promising therapeutic strategy for treatment of benign prostatic hyperplasia
Nahla E El-Ashmawy1,2, Ibrahim M Elazab3, Eman G Khedr1
1Department of Biochemistry, Faculty of Pharmacy, Tanta University, Al-Geish Street, Tanta, El-Gharbia, 31527, Egypt.
Background:
It is still unclear if curcumin's therapeutic effect in benign prostatic hyperplasia (BPH) is linked to microRNA regulation. This study explored the potential role of miR-21-3p in curcumin-induced anti-inflammatory and antiproliferative effects in BPH.
Methods And Results:
Twenty-four male adult rats were grouped randomly into four groups: normal control group, BPH group, BPH group treated with curcumin and BPH group treated with finasteride as a reference drug. The BPH model was experimentally induced by s.c. injection of testosterone enanthate (3 mg/ Kg) five times a week for two weeks, curcumin and finasteride were given orally, parallel to testosterone injection. The results showed that curcumin-induced decrease in prostate index and prostate-specific antigen (PSA)-like protein expression were associated with downregulation of miR-21-3p compared with the BPH untreated group. Immunohistochemical staining revealed increased SIRT1 expression and decreased NF-κB and TNF-α expression in the curcumin-treated group compared to the BPH untreated group. In addition, β-catenin protein expression, measured by Western blotting, as well as β-catenin-linked signaling proteins, LRP6 and c-Myc, were suppressed in the curcumin group. The results obtained with curcumin treatment were comparable to those with finasteride treatment. Our data were supported by histopathological findings.
Conclusions:
The current study demonstrated that curcumin alleviated the inflammatory manifestations of BPH by targeting the pro-inflammatory microRNA miR-21-3p, thereby upregulating SIRT1 and downregulating the pro-inflammatory mediators NF-κB and TNF-α. Furthermore, the anti-proliferative effect of curcumin may be attributed to the inhibition of the β-catenin signaling pathway.
Insights
Curcumin effectively treats benign prostatic hyperplasia (BPH) by targeting miR-21-3p, reducing inflammation via SIRT1, NF-κB, and TNF-α, and inhibiting proliferation through the β-catenin pathway.
Area of Science:
- Biochemistry
- Molecular Biology
- Pharmacology
Background:
- The therapeutic mechanisms of curcumin in benign prostatic hyperplasia (BPH) involving microRNA regulation remain unclear.
- This study investigates the role of miR-21-3p in curcumin's anti-inflammatory and anti-proliferative effects in BPH.
Purpose of the Study:
- To explore the potential role of miR-21-3p in curcumin-induced BPH treatment.
- To elucidate the molecular pathways targeted by curcumin in BPH.
Main Methods:
- A rat model of BPH was established using testosterone enanthate.
- Rats were treated with curcumin or finasteride (reference drug).
- Prostate index, PSA-like protein, miR-21-3p, SIRT1, NF-κB, TNF-α, and β-catenin signaling pathway proteins were analyzed.
Main Results:
- Curcumin treatment downregulated miR-21-3p, decreased prostate index and PSA-like protein.
- Curcumin upregulated SIRT1 and downregulated NF-κB and TNF-α, indicating reduced inflammation.
- Curcumin inhibited β-catenin signaling pathway proteins (LRP6, c-Myc), suggesting antiproliferative effects.
Conclusions:
- Curcumin alleviates BPH inflammation by targeting miR-21-3p, upregulating SIRT1, and downregulating NF-κB and TNF-α.
- Curcumin's antiproliferative effect in BPH is likely mediated by inhibiting the β-catenin signaling pathway.
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