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      Expression of SIRT1 and survivin correlates with poor prognosis in esophageal squamous cell carcinoma

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          Abstract

          This study assessed the association of sirtuin type 1 (SIRT1) and survivin expression with the clinicopathological features and survival of esophageal squamous cell carcinoma (ESCC) patients after concurrent chemoradiotherapy.

          SIRT1 and survivin proteins were immunohistochemically stained in 93 ESCC tissue specimens.

          SIRT1 was expressed in ESCC (80.6% vs 25.8% in normal mucosae) and survivin was expressed in 67.7% of ESCC vs 19.4% normal tissues ( P < .01), and SIRT1 expression was associated with survivin expression (r = 0.39 , P  < .05). Furthermore, expression of both SIRT1 and survivin was associated with tumor size, depth of tumor invasion, tumor differentiation, lymph node metastasis, advanced clinical stage, and chemoradiotherapy ( P < .05) as well as poor progression-free survival (PFS; P  < .05) of ESCC patients after concurrent chemoradiotherapy ( P  < .05). Patient age, chemotherapy, tumor size, clinical stage, lymph node metastasis, and SIRT1 and survivin expression were independent PFS predictors ( P < .05).

          Expression of both SIRT1 and survivin was associated with poor ESCC PFS.

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          Most cited references23

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          Negative control of p53 by Sir2alpha promotes cell survival under stress.

          J. Luo, A Y Nikolaev, S. Imai … (2001)
          The NAD-dependent histone deacetylation of Sir2 connects cellular metabolism with gene silencing as well as aging in yeast. Here, we show that mammalian Sir2alpha physically interacts with p53 and attenuates p53-mediated functions. Nicotinamide (Vitamin B3) inhibits an NAD-dependent p53 deacetylation induced by Sir2alpha, and also enhances the p53 acetylation levels in vivo. Furthermore, Sir2alpha represses p53-dependent apoptosis in response to DNA damage and oxidative stress, whereas expression of a Sir2alpha point mutant increases the sensitivity of cells in the stress response. Thus, our findings implicate a p53 regulatory pathway mediated by mammalian Sir2alpha. These results have significant implications regarding an important role for Sir2alpha in modulating the sensitivity of cells in p53-dependent apoptotic response and the possible effect in cancer therapy.
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            The critical role of the class III histone deacetylase SIRT1 in cancer.

            Tao Liu, P. Liu, John Marshall (2009)
            Gene expression and deacetylase activity of the class III histone deacetylase SIRT1 are up-regulated in cancer cells due to oncogene overexpression or loss of function of tumor suppressor genes. SIRT1 induces histone deacetylation and methylation, promoter CpG island methylation, transcriptional repression, and deacetylation of tumor suppressor proteins. SIRT1 may play a critical role in tumor initiation, progression, and drug resistance by blocking senescence and apoptosis, and promoting cell growth and angiogenesis. SIRT1 inhibitors have shown promising anticancer effects in animal models of cancer. Further screening for more potent SIRT1 inhibitors may lead to compounds suitable for clinical trials in patients.
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              SIRT1 and p53, effect on cancer, senescence and beyond.

              Jingjie Yi, Jianyuan Luo (2010)
              NAD(+)-dependent Class III histone deacetylase SIRT1 is a multiple function protein critically involved in stress responses, cellular metabolism and aging through deacetylating a variety of substrates including p53, forkhead-box transcription factors, PGC-1alpha, NF-kappaB, Ku70 and histones. The first discovered non-histone target of SIRT1, p53, is suggested to play a central role in SIRT1-mediated functions in tumorigenesis and senescence. SIRT1 was originally considered to be a potential tumor promoter since it negatively regulates the tumor suppressor p53 and other tumor suppressors. There is new evidence that SIRT1 acts as a tumor suppressor based on its role in negatively regulating beta-catenin and survivin. This review provides an overview of current knowledge of SIRT1-p53 signaling and controversies regarding the functions of SIRT1 in tumorigenesis. Copyright 2010 Elsevier B.V. All rights reserved.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Medicine (Baltimore)
                Journal ID (iso-abbrev): Medicine (Baltimore)
                Journal ID (publisher-id): MEDI
                Title: Medicine
                Publisher: Lippincott Williams & Wilkins (Hagerstown, MD )
                ISSN (Print): 0025-7974
                ISSN (Electronic): 1536-5964
                Publication date Collection: 21 August 2020
                Publication date (Electronic): 21 August 2020
                Volume: 99
                Issue: 34
                Electronic Location Identifier: e21645
                Affiliations
                [a ]Departments of Oncology, Linyi People's Hospital, Linyi
                [b ]Department of Cell Biology, Shandong University, Jinan
                [c ]Department of Pathology, Linyi People's Hospital, Linyi, China.
                Author notes
                [∗ ]Correspondence: Li Yan, Departments of Oncology, Xuemei Zhan, Department of Pathology, Hospital Linyi People's Hospital, 27 Jiefang Road, Linyi 276003, China (e-mails: yanli1995@ 123456126.com , XM6612@ 123456163.com ).
                Article
                Publisher ID: MD-D-19-09615 Accession ID: 21645
                DOI: 10.1097/MD.0000000000021645
                PMC ID: 7447426
                PubMed ID: 32846774
                SO-VID: 233b275d-f14f-4f8b-ae5e-efc325c9eda7
                Copyright © Copyright © 2020 the Author(s). Published by Wolters Kluwer Health, Inc.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial License 4.0 (CCBY-NC), where it is permissible to download, share, remix, transform, and buildup the work provided it is properly cited. The work cannot be used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc/4.0

                History
                Date received : 4 December 2019
                Date revision received : 26 May 2020
                Date accepted : 28 June 2020
                Funding
                Funded by: Shandong Medical and Health Development Plan
                Award ID: 2014WS0288
                Award Recipient : Li Yan
                Categories
                Subject: 5700
                Subject: Research Article
                Subject: Observational Study
                Custom metadata
                OPEN-ACCESS TRUE

                Keywords: esophageal squamous cell cancer,prognosis,sirtuin type 1,survivin
                Data availability:
                Keywords: esophageal squamous cell cancer, prognosis, sirtuin type 1, survivin

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