Fsk and IBMX inhibit proliferation and proapoptotic of glioma stem cells via activation of cAMP signaling pathway. Issue 1 (1st September 2018)

• Record Type: Journal Article
• Authors: Lv, Peng; Wang, Weiyao; Cao, Zhiyou; Zhao, Donghai; Zhao, Guifang; Li, Dailin; Qi, Ling; Xu, Junjie
• Is Part Of: Journal of cellular biochemistry. Volume 120:Issue 1(2019)
• Page Start: 321
• Page End: 331
• Publication Date: 2018-09-01
• Subjects: cAMP -- Fsk‐IBMX -- GSCs -- MAPK -- proliferation -- signaling pathway; Cytochemistry -- Periodicals; 572
• DOI: 10.1002/jcb.27364
• Languages: English
• ISSNs: 0730-2312

Abstract

Abstract: Objective: We aimed to find out the underlying mechanism of forskolin (Fsk) and 3‐isobutyl‐1‐methylxanthine (IBMX) on glioma stem cells (GSCs). Methods: The expression of cAMP‐related protein CREB and pCREB as well as apoptosis‐related proteins were detected through Western blot analysis. The level of proliferation and growth rate of human GSCs was measured through thiazolyl blue tetrazolium bromide assay and stem cells forming sphere assay. The apoptosis‐related gene expression was measured through reverse transcription‐polymerase chain reaction. Results: cAMP signaling pathway was activated in GSCs with Fsk‐IBMX administration. Fsk‐IBMX could inhibit the proliferation as well as invasion and promote the apoptosis of U87 cells. Besides, U0126 could inhibit MAPK signaling pathway to increase the sensitivity of GSCs to cAMP signaling pathway. As a result, Fsk‐IBMX combined with U0126 had more negative effect on GSCs. Conclusions: The relationship of cAMP and MAPK signaling pathway in GSCs may provide a potential therapeutic strategy in glioma. Abstract : The relationship of cAMP and MAPK signaling pathway in GSCs may provide a potential therapeutic strategy in glioma.