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
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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