A Novel Combination Therapy Approach Targeting STAT3 and Autophagy in Glioblastoma

The aggressive brain cancer glioblastoma (GBM) is notoriously resistant to radiotherapy and chemotherapy, which drives tumor recurrence and relapse. GBM cells are highly addicted to STAT3 (signal transducer and activator of transcription 3) and STAT3 inhibition blocks GBM-driven tumor growth. STAT3...

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Main Authors: Sujoy Bhattacharya, Lawrence M. Pfeffer, Edward Chaum
Format: Article
Language:English
Published: Taylor & Francis Group 2022-12-01
Series:Autophagy Reports
Subjects:
Online Access:http://dx.doi.org/10.1080/27694127.2022.2117340
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author Sujoy Bhattacharya
Lawrence M. Pfeffer
Edward Chaum
author_facet Sujoy Bhattacharya
Lawrence M. Pfeffer
Edward Chaum
author_sort Sujoy Bhattacharya
collection DOAJ
description The aggressive brain cancer glioblastoma (GBM) is notoriously resistant to radiotherapy and chemotherapy, which drives tumor recurrence and relapse. GBM cells are highly addicted to STAT3 (signal transducer and activator of transcription 3) and STAT3 inhibition blocks GBM-driven tumor growth. STAT3 regulates macroautophagy/autophagy, a central player in GBM pathobiology. Although autophagy suppression has been implicated in the pathophysiology of GBM, it is unknown if modulation of autophagy can reduce GBM tumorigenesis. Based on observations from our recent study, the answer appears to be yes, and we propose a therapeutic strategy for dual inhibition of STAT3 and MTOR, or STAT3 and ULK1 to target GBM tumorigenesis and chemoresistance.
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spelling doaj.art-ed062b443e3543afaa92eaf263ca3e112023-09-14T13:24:40ZengTaylor & Francis GroupAutophagy Reports2769-41272022-12-011138538810.1080/27694127.2022.21173402117340A Novel Combination Therapy Approach Targeting STAT3 and Autophagy in GlioblastomaSujoy Bhattacharya0Lawrence M. Pfeffer1Edward Chaum2Vanderbilt University Medical CenterThe Center for Cancer Research, College of Medicine, University of Tennessee Health Science CenterVanderbilt University Medical CenterThe aggressive brain cancer glioblastoma (GBM) is notoriously resistant to radiotherapy and chemotherapy, which drives tumor recurrence and relapse. GBM cells are highly addicted to STAT3 (signal transducer and activator of transcription 3) and STAT3 inhibition blocks GBM-driven tumor growth. STAT3 regulates macroautophagy/autophagy, a central player in GBM pathobiology. Although autophagy suppression has been implicated in the pathophysiology of GBM, it is unknown if modulation of autophagy can reduce GBM tumorigenesis. Based on observations from our recent study, the answer appears to be yes, and we propose a therapeutic strategy for dual inhibition of STAT3 and MTOR, or STAT3 and ULK1 to target GBM tumorigenesis and chemoresistance.http://dx.doi.org/10.1080/27694127.2022.2117340ampkαapoptosiscaspase 3cathepsin dlc3-i/lc3-iimtorc1rad001 (everolimus)ulk1
spellingShingle Sujoy Bhattacharya
Lawrence M. Pfeffer
Edward Chaum
A Novel Combination Therapy Approach Targeting STAT3 and Autophagy in Glioblastoma
Autophagy Reports
ampkα
apoptosis
caspase 3
cathepsin d
lc3-i/lc3-ii
mtorc1
rad001 (everolimus)
ulk1
title A Novel Combination Therapy Approach Targeting STAT3 and Autophagy in Glioblastoma
title_full A Novel Combination Therapy Approach Targeting STAT3 and Autophagy in Glioblastoma
title_fullStr A Novel Combination Therapy Approach Targeting STAT3 and Autophagy in Glioblastoma
title_full_unstemmed A Novel Combination Therapy Approach Targeting STAT3 and Autophagy in Glioblastoma
title_short A Novel Combination Therapy Approach Targeting STAT3 and Autophagy in Glioblastoma
title_sort novel combination therapy approach targeting stat3 and autophagy in glioblastoma
topic ampkα
apoptosis
caspase 3
cathepsin d
lc3-i/lc3-ii
mtorc1
rad001 (everolimus)
ulk1
url http://dx.doi.org/10.1080/27694127.2022.2117340
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