FOXL2-induced follistatin attenuates activin A-stimulated cell proliferation in human granulosa cell tumors

Biochemical and Biophysical Research Communications
Jung-Chien ChengPeter C K Leung

Abstract

Human granulosa cell tumors (GCTs) are rare, and their etiology remains largely unknown. Recently, the FOXL2 402C>G (C134W) mutation was found to be specifically expressed in human adult-type GCTs; however, its function in the development of human GCTs is not fully understood. Activins are members of the transforming growth factor-beta superfamily, which has been shown to stimulate normal granulosa cell proliferation; however, little is known regarding the function of activins in human GCTs. In this study, we examined the effect of activin A on cell proliferation in the human GCT-derived cell line KGN. We show that activin A treatment stimulates KGN cell proliferation. Treatment with the activin type I receptor inhibitor SB431542 blocks activin A-stimulated cell proliferation. In addition, our results show that cyclin D2 is induced by treatment with activin A and is involved in activin A-stimulated cell proliferation. Moreover, the activation of Smad signaling is required for activin A-induced cyclin D2 expression. Finally, we show that the overexpression of the wild-type FOXL2 but not the C134W mutant FOXL2 induced follistatin production. Treatment with exogenous follistatin blocks activin A-stimulated cell proliferation, and ...Continue Reading

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Citations

Feb 18, 2016·Human Reproduction Update·R Wijayarathna, D M de Kretser
Jan 23, 2016·The International Journal of Biochemistry & Cell Biology·Dilys T H LeungSimon Chu
Feb 23, 2018·Endocrinology·Martina BelliShunichi Shimasaki
May 23, 2018·Molecular Human Reproduction·Xin FangQinglei Li
Feb 8, 2018·Journal of Ovarian Research·Jiaheng LiChunping Zhang
Jul 18, 2019·International Journal of Molecular Sciences·Huachen ChenYangXin Fu
Jul 13, 2019·Clinical Cancer Research : an Official Journal of the American Association for Cancer Research·Luisa Bonilla, Amit M Oza

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