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      Autophagy modulation in bladder cancer development and treatment

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          Abstract

          Bladder cancer (BC) is a potentially life-threatening malignancy. Due to a high recurrence rate, frequent surveillance strategies and intravesical drug therapies, BC is considered one of the most expensive tumors to treat. As a fundamental evolutionary catabolic process, autophagy plays an important role in the maintenance of cellular environmental homeostasis by degrading and recycling damaged cytoplasmic components, including macromolecules and organelles. Scientific studies in the last two decades have shown that autophagy acts as a double-edged sword with regard to the treatment of cancer. On one hand, autophagy inhibition is able to increase the sensitivity of cancer cells to treatment, a process known as protective autophagy. On the other hand, autophagy overactivation may lead to cell death, referred to as autophagic cell death, similar to apoptosis. Therefore, it is essential to identify the role of autophagy in cancer cells in order to develop novel therapeutic agents. In addition, autophagy may potentially become a novel therapeutic target in human diseases. In this review, the current knowledge on autophagy modulation in BC development and treatment is summarized.

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          The coordinate regulation of the p53 and mTOR pathways in cells.

          Zhaohui Feng, Haiyan Zhang, Arnold J. Levine … (2005)
          Cell growth and proliferation requires an intricate coordination between the stimulatory signals arising from nutrients and growth factors and the inhibitory signals arising from intracellular and extracellular stresses. Alteration of the coordination often causes cancer. In mammals, the mTOR (mammalian target of rapamycin) protein kinase is the central node in nutrient and growth factor signaling, and p53 plays a critical role in sensing genotoxic and other stresses. The results presented here demonstrate that activation of p53 inhibits mTOR activity and regulates its downstream targets, including autophagy, a tumor suppression process. Moreover, the mechanisms by which p53 regulates mTOR involves AMP kinase activation and requires the tuberous sclerosis (TSC) 1/TSC2 complex, both of which respond to energy deprivation in cells. In addition, glucose starvation not only signals to shut down mTOR, but also results in the transient phosphorylation of the p53 protein. Thus, p53 and mTOR signaling machineries can cross-talk and coordinately regulate cell growth, proliferation, and death.
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            Autophagy and multidrug resistance in cancer

            Ying-Jie Li, Yu-He Lei, Nan Yao … (2017)
            Multidrug resistance (MDR) occurs frequently after long-term chemotherapy, resulting in refractory cancer and tumor recurrence. Therefore, combatting MDR is an important issue. Autophagy, a self-degradative system, universally arises during the treatment of sensitive and MDR cancer. Autophagy can be a double-edged sword for MDR tumors: it participates in the development of MDR and protects cancer cells from chemotherapeutics but can also kill MDR cancer cells in which apoptosis pathways are inactive. Autophagy induced by anticancer drugs could also activate apoptosis signaling pathways in MDR cells, facilitating MDR reversal. Therefore, research on the regulation of autophagy to combat MDR is expanding and is becoming increasingly important. We summarize advanced studies of autophagy in MDR tumors, including the variable role of autophagy in MDR cancer cells.
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              p53 regulates glucose metabolism through an IKK-NF-kappaB pathway and inhibits cell transformation.

              Keiko Kawauchi, Keigo Araki, Kei Tobiume … (2008)
              Cancer cells use aerobic glycolysis preferentially for energy provision and this metabolic change is important for tumour growth. Here, we have found a link between the tumour suppressor p53, the transcription factor NF-kappaB and glycolysis. In p53-deficient primary cultured cells, kinase activities of IKKalpha and IKKbeta and subsequent NF-kappaB activity were enhanced. Activation of NF-kappaB, by loss of p53, caused an increase in the rate of aerobic glycolysis and upregulation of Glut3. Oncogenic Ras-induced cell transformation and acceleration of aerobic glycolysis in p53-deficient cells were suppressed in the absence of p65/NF-kappaB expression, and were restored by GLUT3 expression. It was also shown that a glycolytic inhibitor diminished the enhanced IKK activity in p53-deficient cells. Moreover, in Ras-expressing p53-deficient cells, IKK activity was suppressed by p65 deficiency and restored by GLUT3 expression. Taken together, these data indicate that p53 restricts activation of the IKK-NF-kappaB pathway through suppression of glycolysis. These results suggest that a positive-feedback loop exists, whereby glycolysis drives IKK-NF-kappaB activation, and that hyperactivation of this loop by loss of p53 is important in oncogene-induced cell transformation.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Oncol Rep
                Journal ID (iso-abbrev): Oncol. Rep
                Title: Oncology Reports
                Publisher: D.A. Spandidos
                ISSN (Print): 1021-335X
                ISSN (Electronic): 1791-2431
                Publication date (Print): November 2019
                Publication date (Electronic): 21 August 2019
                Publication date PMC-release: 21 August 2019
                Volume: 42
                Issue: 5
                Pages: 1647-1655
                Affiliations
                Department of Urology, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China
                Author notes
                Correspondence to: Dr Honglan Zhou, Department of Urology, The First Hospital of Jilin University, 71 Xinmin Street, Changchun, Jilin 130021, P. R. China, E-mail: walkerzhouhl@ 123456163.com
                Article
                Publisher ID: OR-0-0-7286
                DOI: 10.3892/or.2019.7286
                PMC ID: 6775810
                PubMed ID: 31436298
                SO-VID: e22de855-87a9-4baf-82e6-71fc8f4f8c8f
                Copyright © Copyright: © Li et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                Date received : 24 April 2019
                Date accepted : 01 August 2019
                Categories
                Subject: Review

                Keywords: autophagy,bladder cancer,autophagosome,lysosome,autophagic cell death
                Data availability:
                Keywords: autophagy, bladder cancer, autophagosome, lysosome, autophagic cell death

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