RESUMEN
Follicle-stimulating hormone (FSH) is a pituitary glycoprotein that regulates follicle maturation through its binding to follicle-stimulating hormone receptor (FSHR). Endothelial cells express FSHR, but its exact role in endothelial cells remains unclear. Here we show that FSHR expression was detectable in human umbilical vein endothelial cells (HUVECs). FSH stimulation promoted HUVECs migration but not proliferation. Because FSHR is a GPCR, FSH treatment triggers the activation of cAMP-PKA signaling pathways, and the JAK-STAT, PI3K-AKT, and JNK-MAPK pathways. RNAi of FSHR dramatically attenuated the activation effect of FSH on HUVECs migration, as well as the related signaling pathways. Treatment of FSH in HUVECs also transcriptionally upregulated the expression of VAV3 and LAMA2, suppression either of VAV3 or LAMA2 by RNAi attenuated the FSH's effect on HUVECs migration. All of these results indicated a functional role of FSH in the regulation of endothelial cells.
Asunto(s)
Movimiento Celular , Hormona Folículo Estimulante Humana/metabolismo , Hormona Folículo Estimulante , Receptores de HFE/metabolismo , Células Endoteliales de la Vena Umbilical Humana/metabolismo , Humanos , Fosfatidilinositol 3-Quinasas/metabolismo , Receptores de HFE/genética , Transducción de SeñalRESUMEN
The phosphatidylinositol 3kinase (PI3K)/protein kinase B (AKT) signaling pathway is involved in the regulation of multiple cellular physiological processes by activating downstream corresponding effector molecules, which serve an important role in the cell cycle, growth and proliferation. This is a common phenomenon; overactivation of the pathway is present in human malignancies and has been implicated in cancer progression, hence one of the important approaches to the treatment of tumors is rational drug design using molecular targets in the PI3K/AKT signaling pathway. In brief, the present review analyzed the effects of the PI3K/AKT signaling pathway on certain gynecological cancer types.
