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Fsk and IBMX inhibit proliferation and proapoptotic of glioma stem cells via activation of cAMP signaling pathway
Author(s) -
Lv Peng,
Wang Weiyao,
Cao Zhiyou,
Zhao Donghai,
Zhao Guifang,
Li Dailin,
Qi Ling,
Xu Junjie
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27364
Subject(s) - ibmx , microbiology and biotechnology , stem cell , cancer research , signal transduction , chemistry , biology , biochemistry , forskolin , in vitro
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.