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Combination of All-trans Retinoic Acid and Interferon-gamma Suppressed PI3K/Akt Survival Pathway in Glioblastoma T98G Cells whereas NF-κB Survival Signaling in Glioblastoma U87MG Cells for Induction of Apoptosis

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Combination of All-trans Retinoic Acid and Interferon-gamma Suppressed PI3K/Akt Survival Pathway in Glioblastoma T98G Cells whereas NF-κB Survival Signaling in Glioblastoma U87MG Cells for Induction of Apoptosis

Content Provider	Springer Nature Link
Author	Zhang, Ran Banik, Naren L. Ray, Swapan K.
Copyright Year	2007
Abstract	Phosphatase and tension homolog located on chromosome ten (PTEN) is a tumor suppressor as it negatively regulates activation of Akt. Mutation or deletion of PTEN has been found in as high as 80% of glioblastomas, which harbor aberrant cell signaling passing through the phosphatidylinositol-3-kinase (PI3K) and Akt (PI3K/Akt) survival pathway. Glioblastoma cells without functional PTEN are not easily amenable to apoptosis. We investigated the possibility of modulation of signal transduction pathways for induction of apoptosis in human glioblastoma T98G (PTEN-harboring) and U87MG (PTEN-deficient) cell lines after treatment with the combination of all-trans retinoic acid (ATRA) and interferon-gamma (IFN-γ). Treatment with ATRA plus IFN-γ stimulated PTEN expression and suppressed Akt activation in T98G cells, whereas no PTEN expression but Akt activation in U87MG cells under the same conditions. Pretreatment of U87MG cells with the PI3K inhibitor LY294002 could prevent Akt activation. Interestingly, ATRA plus IFN-γ could significantly decrease cell viability and increase morphological features of apoptosis in both cell lines. Combination of ATRA and IFN-γ showed more efficacy than IFN-γ alone in causing apoptosis that occurred due to increases in Bax:Bcl-2 ratio, mitochondrial release of cytochrome c, and caspase-3 activity. Luciferase reporter gene assay showed that combination of ATRA and IFN-γ significantly down regulated transcriptional activity of the nuclear factor kappa B (NF-κB), a survival signaling factor, in U87MG cells. Thus, combination of ATRA and IFN-γ caused significant amounts of apoptosis in T98G cells due to suppression of the PI3K/Akt survival pathway while the same treatment caused apoptosis in U87MG cells due to down regulation of the NF-κB activity. Therefore, the combination of ATRA and IFN-γ could modulate different survival signal transduction pathways for induction of apoptosis and should be considered as an effective therapeutic strategy for controlling the growth of both PTEN-harboring and PTEN-deficient glioblastomas.
Starting Page	2194
Ending Page	2202
Page Count	9
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	32
Issue Number	12
e-ISSN	15736903
Language	English
Publisher	Springer US
Publisher Date	2007-07-07
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Apoptosis ATRA Glioblastoma IFN-γ Luciferase reporter gene assay NF-κB activity PI3K/Akt survival pathway Neurology Biochemistry Neurosciences
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

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Combination of All-trans Retinoic Acid and Interferon-gamma Suppressed PI3K/Akt Survival Pathway in Glioblastoma T98G Cells whereas NF-κB Survival Signaling in Glioblastoma U87MG Cells for Induction of Apoptosis

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Combination of All-trans Retinoic Acid and Interferon-gamma Suppressed PI3K/Akt Survival Pathway in Glioblastoma T98G Cells whereas NF-κB Survival Signaling in Glioblastoma U87MG Cells for Induction of Apoptosis