Basic & Clinical Medicine ›› 2026, Vol. 46 ›› Issue (1): 39-45.doi: 10.16352/j.issn.1001-6325.2026.01.0039

• Original Articles • Previous Articles     Next Articles

Berberine enhances the chemotherapy sensitivity of prostate cancer cell line 22RV1 to docetaxel

LU Wei1*, WANG Yanmin1, LIU Bingchen1, TAO Xin1, WANG Shipeng1, CAO Qiuye2   

  1. 1. Department of Urology, Jilin Provincial People's Hospital, Changchun 130021;
    2. Department of Thoracic and Urology, Qian'an County People's Hospital, Songyuan 131499, China
  • Received:2025-01-07 Revised:2025-04-28 Online:2026-01-05 Published:2025-12-29
  • Contact: *wkkki2@163.com

Abstract: Objective To investigate the chemotherapy effectiveness of berberine (BBR) to enhance sensitivity of prostate cancer cell line 22RV1 to docetaxel. Methods The docetaxel (DTX) resistant cell was constructed using prostate cancer cell line 22RV1. The drug-resistant cell strain(22RV1/DTX) was divided into: 22RV1/DTX group, low concentration (L)-BBB+22RV1/DTX group, high concentration (H)-BBB+22RV1/DTX group and H-BBR+ERK activator+22RV1/DTX group. CCK8 method was applied to detect cell proliferation. Scratch healing test was applied to detect migration. Transwell test was applied to detect invasion. Flow cytometry was applied to detect apoptosis. Western blot was applied to detect the expression of extra-cellular regulated protein kinases (ERK), pERK, and ETS transcription factor (ELK1) proteins in cells. Results Compared with 22RV1/DTX group, the proliferation, migration, and invasion of cells in the L-BBR+22RV1/DTX group and H-BBR+22RV1/DTX group were lower but the apoptosis rate was higher (P<0.05). The proliferation, migration, and invasion of cells in the H-BBR+ERK activator+22RV1/DTX group were higher, and the apoptosis rate was lower (P<0.05). BBR significantly reduced the pERK/ERK ratio and ELK1 protein expression level in 22RV1/DTX cells(P<0.05).The effects on 22RV1/DTX cells and pathways were reversed by ERK activator (P<0.05). Conclusions BBR may inhibit the proliferation, migration, and invasion of drug-resistant cells, promote cell apoptosis and thus enhance the chemotherapy sensitivity of prostate cancer cells to DTX with underlying mechanism of suppressing the ERK/ELK1 signaling pathway.

Key words: berberine, ERK/ELK1, prostate cancer cell, chemotherapy sensitivity

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