Metformin mitigates PLCε gene expression and modulates the Notch1/Hes and androgen receptor signaling pathways in castration‑resistant prostate cancer xenograft models
- Qi Li
- Ke Xu
- Jianguo Tian
- Zhicheng Lu
- Jianming Pu
Affiliations: Department of Urology, Changshu Hospital Affiliated to Nanjing University of Chinese Medicine, Suzhou, Jiangsu 215500, P.R. China
- Published online on: August 8, 2021 https://doi.org/10.3892/ol.2021.12976
Copyright: © Li
et al. This is an open access article distributed under the
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Commons Attribution License.
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The present study aimed to establish a mouse model of patient‑derived castration‑resistant prostate cancer (CRPC) xenograft tumors, and to evaluate the effects of various doses of metformin on phospholipase Cε (PLCε) expression and the neurogenic locus notch homolog protein 1 (Notch1)/hairy and enhancer of split 1 and androgen receptor (AR) signaling pathways via western blotting and reverse transcription‑quantitative PCR. Additionally, phorbol 12‑myristate 13‑acetate was used to activate PLC, and Jagged1 was used as a Notch activator to verify whether metformin could suppress CRPC development via the PLCε/Notch1/AR pathways. The results confirmed that metformin may serve critical roles in CRPC by significantly inhibiting the occurrence, growth and proliferation of CRPC tumors by decreasing PLCε/Notch1 expression and AR nucleation.