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      Demethoxycurcumin analogue DMC-BH inhibits orthotopic growth of glioma stem cells by targeting JNK/ERK signaling

      research-article
      Author(s): 1 , 2 , , 3
      Publication date (Electronic):
      Journal: Aging (Albany NY)
      Publisher: Impact Journals
      Keywords: DMC-BH, JNK, ERK, apoptosis, autophagy, proliferation

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          Abstract

          Glioma stem cells (GSCs) play an important role in glioblastoma resistance to conventional therapies and disease recurrence. Here, we assessed the therapeutic effect of a demethoxycurcumin analogue, DMC-BH, on GSCs, and investigated the underlying mechanisms. Our in vitro data demonstrate that DMC-BH inhibits GSC proliferation, and induces apoptosis and autophagy in GSCs. In addition, our results show that DMC-BH effectively crosses the blood-brain barrier to inhibit the growth of intracranial GSC tumors in vivo. DMC-BH significantly increased phosphorylation levels of JNK, ERK and c-Jun in GSCs. Inhibition of JNK and ERK activities reversed the pro-apoptotic effect of DMC-BH in GSCs, indicating that the DMC-BH-induced apoptosis in GSCs is mediated via the JNK/ERK signaling pathway. These results suggest that DMC-BH could potentially serve as a effective therapy against GSCs that acts by targeting the JNK/ERK signaling pathway.

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          Signaling pathway of MAPK/ERK in cell proliferation, differentiation, migration, senescence and apoptosis.

          Yu-Chen Sun, Wen-Zhou Liu, Tao Liu … (2015)
          The generic mitogen-activated protein kinases (MAPK) signaling pathway is shared by four distinct cascades, including the extracellular signal-related kinases (ERK1/2), Jun amino-terminal kinases (JNK1/2/3), p38-MAPK and ERK5. Mitogen-activated protein kinases/extracellular signal-regulated kinase (MAPK/ERK) pathway is reported to be associated with the cell proliferation, differentiation, migration, senescence and apoptosis. The literatures were searched extensively and this review was performed to review the role of MAPK/ERK signaling pathway in cell proliferation, differentiation, migration, senescence and apoptosis.
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            Role of autophagy in temozolomide-induced cytotoxicity for malignant glioma cells.

            T Kanzawa, I Germano, T Komata … (2004)
            Autophagy is originally named as a process of protein recycling. It begins with sequestering cytoplasmic organelles in a membrane vacuole called autophagosome. Autophagosomes then fuse with lysosomes, where the materials inside are degraded and recycled. To date, however, little is known about the role of autophagy in cancer therapy. In this study, we present that temozolomide (TMZ), a new alkylating agent, inhibited the viability of malignant glioma cells in a dose-dependent manner and induced G2/M arrest. At a clinically achievable dose (100 microM), TMZ induced autophagy, but not apoptosis in malignant glioma cells. After the treatment with TMZ, microtubule-associated protein light-chain 3 (LC3), a mammalian homologue of Apg8p/Aut7p essential for amino-acid starvation-induced autophagy in yeast, was recruited on autophagosome membranes. When autophagy was prevented at an early stage by 3-methyladenine, a phosphatidylinositol 3-phosphate kinase inhibitor, not only the characteristic pattern of LC3 localization, but also the antitumor effect of TMZ was suppressed. On the other hand, bafilomycin A1, a specific inhibitor of vacuolar type H(+)-ATPase, that prevents autophagy at a late stage by inhibiting fusion between autophagosomes and lysosomes, sensitized tumor cells to TMZ by inducing apoptosis through activation of caspase-3 with mitochondrial and lysosomal membrane permeabilization, while LC3 localization pattern stayed the same. These results indicate that TMZ induces autophagy in malignant glioma cells. Application of an autophagy inhibitor that works after the association of LC3 with autophagosome membrane, such as bafilomycin A1, is expected to enhance the cytotoxicity of TMZ for malignant gliomas.
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              Targeting autophagy to sensitive glioma to temozolomide treatment

              Yuanliang Yan, Zhijie Xu, Shuang-Shuang Dai … (2016)
              Temozolomide (TMZ), an alkylating agent, is widely used for treating primary and recurrent high-grade gliomas. However, the efficacy of TMZ is often limited by the development of resistance. Recently, studies have found that TMZ treatment could induce autophagy, which contributes to therapy resistance in glioma. To enhance the benefit of TMZ in the treatment of glioblastomas, effective combination strategies are needed to sensitize glioblastoma cells to TMZ. In this regard, as autophagy could promote cell survival or autophagic cell death, modulating autophagy using a pharmacological inhibitor, such as chloroquine, or an inducer, such as rapamycin, has received considerably more attention. To understand the effectiveness of regulating autophagy in glioblastoma treatment, this review summarizes reports on glioblastoma treatments with TMZ and autophagic modulators from in vitro and in vivo studies, as well as clinical trials. Additionally, we discuss the possibility of using autophagy regulatory compounds that can sensitive TMZ treatment as a chemotherapy for glioma treatment.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Aging (Albany NY)
                Journal ID (iso-abbrev): Aging (Albany NY)
                Journal ID (publisher-id): Aging
                Title: Aging (Albany NY)
                Publisher: Impact Journals
                ISSN (Electronic): 1945-4589
                Publication date Collection: 31 July 2020
                Publication date (Electronic): 24 July 2020
                Volume: 12
                Issue: 14
                Pages: 14718-14735
                Affiliations
                [1 ]Department of Neurosurgery, Affiliated Kunshan Hospital of Jiangsu University, Suzhou 215300, P.R.China
                [2 ]Department of Neurosurgery, The Fourth Affiliated Hospital of Nantong University, Yancheng No.1 People's Hospital, Yancheng 224000, P. R. China
                [3 ]Department of Neurosurgery, Funing People’s Hospital, Funing 224400, P.R.China
                Author notes
                [*]

                Equal contribution

                Correspondence to: Guan Sun; email: sunguan2008@sina.com
                Article
                Publisher ID: 103531 Publisher ID: 103531
                DOI: 10.18632/aging.103531
                PMC ID: 7425509
                PubMed ID: 32710727
                SO-VID: 600fb749-96aa-4b72-adb5-ee983b464b1e
                Copyright © Copyright © 2020 Shi et al.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 10 November 2019
                Date accepted : 20 May 2020
                Categories
                Subject: Research Paper

                ScienceOpen disciplines: Cell biology
                Keywords: dmc-bh,jnk,erk,apoptosis,autophagy,proliferation
                Data availability:
                ScienceOpen disciplines: Cell biology
                Keywords: dmc-bh, jnk, erk, apoptosis, autophagy, proliferation

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