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Estrogen affects cell growth and IGF-1 receptor expression in renal cell carcinoma

Authors Sun L, Gao Z, Luo L, Tan H, Zhang G

Received 24 April 2018

Accepted for publication 29 June 2018

Published 17 September 2018 Volume 2018:11 Pages 5873—5878

DOI https://doi.org/10.2147/OTT.S172149

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Andrew Yee

Peer reviewer comments 4

Editor who approved publication: Dr Federico Perche


Lijiang Sun,* Zhemin Gao,* Lei Luo, Hailin Tan, Guiming Zhang

Department of Urology, The Affiliated Hospital of Qingdao University, Qingdao, People’s Republic of China

*These authors contributed equally to this work

Purpose: Both obesity and gender are important etiological factors in renal cell carcinoma (RCC) development, suggesting a pivotal role of sex hormone signaling pathway and insulin-like growth factor (IGF) family in RCC carcinogenesis. Here, we aimed to investigate the effect of estrogen on RCC growth and the possible interaction between estrogen/estrogen receptor (ER) signaling pathway and the IGF axis.
Methods: ER-α and ER-β were detected in four human RCC cell lines. Cells were treated with 17β-estradiol (E2), and cell proliferation was determined using the cell counting kit-8 assay. Using siRNA, ER-β was downregulated in RCC cells and the effect of E2 on cell growth and IGF-1 receptor (IGF-1R) expression was examined.
Results: E2 inhibited 786-O cell but not A498 cell growth significantly. After the downregulation of ER-β, E2 showed no obvious inhibitory role in 786-O cells. E2 stimulation increased the expression of IGF-1R in 786-O cells. Downregulation of ER-β, as well as fulvestrant, attenuated the stimulatory effect of E2 on IGF-1R expression.
Conclusion: Our results revealed that estrogen induced RCC growth inhibition via an ER-β-dependent pathway. Estrogen also upregulated the expression of IGF-1R, suggesting a link between estrogen/ER and IGF axis.

Keywords:
renal cell carcinoma, estrogen, insulin-like growth factor-1 receptor

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