Estrogen enhances the proliferation and migration of ovarian cancer cells by activating transient receptor potential channel C3
| Autor: | Jia Li, Xiaohua Hao, Rou-Gang Xie, Chu Wenguang, Kuo Jiang, Shengnan Li, Yuanyuan Zhu, Ceng Luo, Biliang Chen |
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| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
endocrine system diseases medicine.drug_class Stimulation Transfection lcsh:Gynecology and obstetrics 03 medical and health sciences Transient receptor potential channel 0302 clinical medicine TRPC3 Cell Movement Cell Line Tumor medicine Humans Gene silencing lcsh:RG1-991 Cell Proliferation Ovarian Neoplasms Messenger RNA Mechanism (biology) Chemistry Research Obstetrics and Gynecology Estrogens Complement C3 Epithelial ovarian cancer medicine.disease Estrogen female genital diseases and pregnancy complications 030104 developmental biology Transient receptor potential channel C3 (TRPC3) Oncology Cell proliferation cell migraiton 030220 oncology & carcinogenesis Cancer research Female Ovarian cancer |
| Zdroj: | Journal of Ovarian Research Journal of Ovarian Research, Vol 13, Iss 1, Pp 1-11 (2020) |
| ISSN: | 1757-2215 |
| DOI: | 10.1186/s13048-020-00621-y |
| Popis: | Background Recent studies have suggested that estrogen (E2) plays an important role in epithelial ovarian cancer (EOC). However, the mechanism of E2 in ovarian cancers is unclear. The purpose of this study was to investigate the effect of E2 on ovarian cancers and illuminate the mechanism of E2 in promote ovarian cancers proliferation. Results We demonstrated that E2 stimulated the proliferation and invasion of ovarian cancer cells. In this study, ovarian cancer specimens were also analyzed for transient receptor potential channel C3 (TRPC3) expression; TRPC3 expression levels were higher in ovarian cancer samples than in normal ovarian tissue samples. Previous studies have shown that TRPC3 contributes to the progression of human ovarian cancer. In this study, we further investigated the interaction between E2 and TRPC3. We found that E2 stimulation enhanced the expression of TRPC3 at both the mRNA and protein levels. E2 stimulation enhanced the influx of Ca2+. Moreover, siRNA-mediated silencing of TRPC3 expression inhibited the ability of E2 to stimulate the influx of Ca2+. Conclusions In conclusion, TRPC3 plays a significant role in the stimulatory activity of E2 and could be a therapeutic target for the treatment of EOC. Furthermore, this study elucidates the molecular mechanism by which E2 promotes the proliferation and migration of EOC cells. |
| Databáze: | OpenAIRE |
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