| ORIGINAL ARTICLE |
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| Year : 2020 | Volume
: 16
| Issue : 69 | Page : 435-440 |
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Formononetin induces apoptosis of PC-3 human prostate cancer cells via regulating long noncoding RNA H19 and the mitochondrial apoptosis pathway
Ruyue Wang1, Kaiguo Li2, Zhaodi Xie3, Bailei Wang4, Yan Dai5, Jian Chen5, Yu Ye1
1 Department of Emergency, Second Affiliated Hospital of Guangxi Medical University, Nanning, China
2 Department of Radiation Oncology, Affiliated Cancer Hospital of Guangxi Medical University, Cancer Institute of Guangxi Zhuang Autonomous Region, Nanning, China
3 Department of Burns and Cutaneous Surgery, Xijing Hospital, Xi'an, Shaanxi, China
4 Medical Emergency Center, Beihai People's Hospital, Beihai, China
5 Department of Physiology, Faculty of Basic Medicine, Guilin Medical University, Guilin, Guangxi, China
Correspondence Address:
Yu Ye
Department of Emergency, Second Affiliated Hospital of Guangxi Medical University, Shuangyong Road No. 22, Nanning 530021, Guangxi
China
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/pm.pm_320_19
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Background: Prostate cancer is a life-threating disease with high incidence and mortality in male. Formononetin, the main active component of some natural products, has been hypothesized as a promising anticancer agent in previous studies. Objectives: We investigated the toxic effects and potential molecular mechanism of formononetin in PC-3 prostate cancer cells to further understand the pharmacological effects of formononetin and provide more references for intensive research. Materials and Methods: PC-3 cells were incubated with different doses of formononetin for 24 h or 48 h. After that, cell viability was measured by Cell Counting Kit-8, and apoptosis was analyzed by Hoechst 33258 stains. The expression levels of tumor-related factors such as long noncoding RNA (LncRNA) H19, Bax, and Bcl-2 were determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blot methods. Subsequently, PC-3 cells were infected with a lentiviral vector to overexpress or knock down H19, and then, the expression of insulin-like growth factor-1 receptor (IGF-1R) mRNA was measured by RT-qPCR. Results: Formononetin significantly inhibited the viability of PC-3 cells and promoted apoptosis in a time-dose-dependent manner. We observed that the expressions of lncRNA H19 and Bcl-2 were significantly downregulated compared with the untreated group, while an opposite pattern was observed for Bax. According to the results of gene interaction experiments, IGF-1R may be a downstream target of H19 in PC-3 cells. Conclusion: Our results present evidence that formononetin induced apoptosis of PC-3 cells by regulating lncRNA H19 and the mitochondrial apoptosis pathway. Furthermore, we put forward the hypothesis that formononetin has an interference effect on the H19/IGF-1R pathway, which remains to be further confirmed.
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