Insulin-Like Growth Factor-1 Promotes Human Uterine Leiomyoma Cell Proliferation via PI3K/AKT/mTOR Pathway

Abstract

The present research aimed to evaluate the expression of insulin-like growth factor-1 (IGF-1) in uterine leiomyoma, and explore its relationship with the occurrence and development of uterine leiomyoma and potential signal pathways. qRT-PCR and enzyme-linked immunosorbent assay were used for estimating the levels of IGF-1 in human uterine leiomyoma compared to myometrium. The expression of cell proliferation and PI3K/AKT/mTOR signaling pathway-related proteins in uterine leiomyoma cells was evaluated by western blot. Cell viability analysis was performed by CCK-8 assay. Lentivirus infection was used for IGF-1 overexpression and knockdown in uterine leiomyoma cells. The IGF-1 expression level was elevated in human uterine leiomyomas compared to myometrium. IGF-1 promoted the cell viability of human uterine leiomyoma cells. Overexpression of IGF-1 induced the expression of pro-proliferation markers including c-Myc, PCNA, and cyclin D1 in uterine leiomyoma cells. IGF-1 elevated the phosphorylation levels of PI3K, AKT, and mTOR, thus modifying PI3K/AKT/mTOR signaling in uterine leiomyoma cells. IGF-1 promotes proliferation of human uterine leiomyoma cells via PI3K/AKT/mTOR pathway.

Keywords: Insulin-like growth factor-1; PI3K/AKT/mTOR signaling pathway; Uterine leiomyomas.