1. Academic Validation
  2. Fsk and IBMX inhibit proliferation and proapoptotic of glioma stem cells via activation of cAMP signaling pathway

Fsk and IBMX inhibit proliferation and proapoptotic of glioma stem cells via activation of cAMP signaling pathway

  • J Cell Biochem. 2019 Jan;120(1):321-331. doi: 10.1002/jcb.27364.
Peng Lv 1 Weiyao Wang 1 Zhiyou Cao 2 Donghai Zhao 3 Guifang Zhao 3 Dailin Li 4 Ling Qi 1 Junjie Xu 5
Affiliations

Affiliations

  • 1 Department of Pathophysiology, Jilin Medical University, Jilin, China.
  • 2 465 Hospital, Jilin Medical University, Jilin, China.
  • 3 Department of Pathology, Jilin Medical University, Jilin, China.
  • 4 Institute of Petrochemical Technology, Jilin Institute of Chemical Technology, Jilin, China.
  • 5 School of Basic Medicine Sciences, Jilin Medical University, Jilin, China.
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.

Keywords

Fsk-IBMX; GSCs; MAPK; cAMP; proliferation; signaling pathway.

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