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


Journal

Journal of cellular biochemistry
ISSN: 1097-4644
Titre abrégé: J Cell Biochem
Pays: United States
ID NLM: 8205768

Informations de publication

Date de publication:
01 2019
Historique:
received: 14 11 2017
accepted: 26 06 2018
pubmed: 2 9 2018
medline: 26 2 2020
entrez: 2 9 2018
Statut: ppublish

Résumé

We aimed to find out the underlying mechanism of forskolin (Fsk) and 3-isobutyl-1-methylxanthine (IBMX) on glioma stem cells (GSCs). 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. 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. The relationship of cAMP and MAPK signaling pathway in GSCs may provide a potential therapeutic strategy in glioma.

Identifiants

pubmed: 30171713
doi: 10.1002/jcb.27364
doi:

Substances chimiques

Butadienes 0
CREB1 protein, human 0
Cyclic AMP Response Element-Binding Protein 0
Nitriles 0
Plant Extracts 0
U 0126 0
Colforsin 1F7A44V6OU
Cyclic AMP E0399OZS9N
Mitogen-Activated Protein Kinases EC 2.7.11.24
1-Methyl-3-isobutylxanthine TBT296U68M

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

321-331

Informations de copyright

© 2018 Wiley Periodicals, Inc.

Auteurs

Peng Lv (P)

Department of Pathophysiology, Jilin Medical University, Jilin, China.

Weiyao Wang (W)

Department of Pathophysiology, Jilin Medical University, Jilin, China.

Zhiyou Cao (Z)

465 Hospital, Jilin Medical University, Jilin, China.

Donghai Zhao (D)

Department of Pathology, Jilin Medical University, Jilin, China.

Guifang Zhao (G)

Department of Pathology, Jilin Medical University, Jilin, China.

Dailin Li (D)

Institute of Petrochemical Technology, Jilin Institute of Chemical Technology, Jilin, China.

Ling Qi (L)

Department of Pathophysiology, Jilin Medical University, Jilin, China.

Junjie Xu (J)

School of Basic Medicine Sciences, Jilin Medical University, Jilin, China.

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Classifications MeSH