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      FHIT down-regulation was inversely linked to aggressive behaviors and adverse prognosis of gastric cancer: a meta- and bioinformatics analysis

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      Author(s): 1 , 2
      Publication date (Electronic):
      Journal: Oncotarget
      Publisher: Impact Journals LLC
      Keywords: FHIT, gastric cancer, meta-analysis, bioinformatics analysis

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          Abstract

          FHIT (fragile histine triad) acts as diadenosine P1, P3-bis (5'-adenosyl)-triphosphate adenylohydrolase involved in purine metabolism, and induces apoptosis as a tumor suppressor. We performed a systematic meta- and bioinformatics analysis through multiple online databases up to March 14, 2017. The down-regulated FHIT expression was found in gastric cancer, compared with normal mucosa and dysplasia ( p < 0.05). FHIT expression was negatively with depth of invasion, lymph node metastasis, distant metastasis, TNM staging and dedifferentiation of gastric cancer ( p < 0.05). A positive association between FHIT expression and favorable overall survival was found in patients with gastric cancer ( p < 0.05). According to Kaplan-Meier plotter, we found that a higher FHIT expression was negatively correlated with overall and progression-free survival rates of all cancer patients, even stratified by aggressive parameters ( p < 0.05). These findings indicated that FHIT expression might be employed as a potential marker to indicate gastric carcinogenesis and subsequent progression, even prognosis.

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          Most cited references68

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          Tumour suppressor gene expression correlates with gastric cancer prognosis.

          Koth-Bong-Woo-Ri Kim, Norman Lee, Han-Soeb Yang … (2003)
          The loss of tumour suppressor genes (TSGs) is a key event in many human cancers, including gastric carcinoma. Many TSG candidates have been studied, but their roles in gastric carcinogenesis remain unclear. To clarify the clinical significance of TSG expression in gastric carcinoma, the expression of various TSG candidates (p53, E-cadherin, FHIT, smad4, rb, VHL, PTEN, MGMT, p16, and KAI1), as well as other proteins (bcl-2, MUC1, MUC2, MUC5AC, MUC6, CEA, CD44, beta-catenin, C-erbB2, and cyclin B2), was evaluated immunohistochemically in 329 consecutive gastric carcinomas using the tissue array method. The overexpression of p53 and MUC1 (p < 0.01) and the loss of expression of smad4 (p = 0.04), FHIT (p = 0.03), MGMT (p = 0.01), E-cadherin, KAI1, and PTEN (p < 0.01) were found to be significantly associated with poor gastric carcinoma prognosis. Seven out of eight survival-associated proteins were found to be protein products of TSGs. The gastric carcinomas were divided into five groups according to the grade of alteration in TSG expression. No TSG expression loss was found in 32 cases (TSG1). One TSG loss was found in 47 cases (TSG2), two in 67 cases (TSG3), three or four in 64 cases (TSG4), and five, six, or seven in 38 cases (TSG5). The grade of TSG expression was confirmed to be significantly associated with WHO classification (p = 0.04), pTNM stage, lymphatic invasion, and patient survival (p < 0.01 for the latter three). By multivariate analysis, the grade of TSG expression was found to be significantly and independently associated with patient survival (p < 0.01). In conclusion, the findings of this study suggest that the cumulative loss of TSG expression in gastric carcinoma is important in determining patient survival. Copyright 2003 John Wiley & Sons, Ltd.
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            The FHIT gene product: tumor suppressor and genome "caretaker".

            Catherine Waters, Joshua Saldivar, Seyed Hosseini … (2014)
            The FHIT gene at FRA3B is one of the earliest and most frequently altered genes in the majority of human cancers. It was recently discovered that the FHIT gene is not the most fragile locus in epithelial cells, the cell of origin for most Fhit-negative cancers, eroding support for past claims that deletions at this locus are simply passenger events that are carried along in expanding cancer clones, due to extreme vulnerability to DNA damage rather than to loss of FHIT function. Indeed, recent reports have reconfirmed FHIT as a tumor suppressor gene with roles in apoptosis and prevention of the epithelial-mesenchymal transition. Other recent works have identified a novel role for the FHIT gene product, Fhit, as a genome "caretaker." Loss of this caretaker function leads to nucleotide imbalance, spontaneous replication stress, and DNA breaks. Because Fhit loss-induced DNA damage is "checkpoint blind," cells accumulate further DNA damage during subsequent cell cycles, accruing global genome instability that could facilitate oncogenic mutation acquisition and expedite clonal expansion. Loss of Fhit activity therefore induces a mutator phenotype. Evidence for FHIT as a mutator gene is discussed in light of these recent investigations of Fhit loss and subsequent genome instability.
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              Mixed-type gastric carcinomas exhibit more aggressive features and indicate the histogenesis of carcinomas

              Hua-chuan Zheng, Xiao-han Li, Takuo Hara … (2008)
              To investigate the pathobiological behaviors of gastric mixed-type (MT) carcinomas and gastric carcinogenesis, the clinicopathological characteristics of MT carcinomas were analyzed and compared with intestinal-type (IT) and diffuse-type (DT) carcinomas. The expression of Ki-67, caspase-3, p53, fragile histine triad (FHIT), maspin, extracellular matrix metalloproteinase inducer (EMMPRIN), vascular growth factor (VEGF), MUC-2, 4, 5AC and 6, CD44, E-cadherin, β-catenin, and phosphorylated glycogen synthase kinase 3β-ser9 (P-GSK3β-ser9) was examined on tissue microarrays using immunohistochemistry. It was found that MT carcinomas exhibited large size, deep invasion, frequent local invasion, and lymph node metastasis in comparison with IT and DT carcinomas (p < 0.05). All the markers except MUC-5AC showed higher expression in IT than DT carcinomas (p < 0.05). The expression of maspin, EMMPRIN, VEGF, MUC-4, and membrane E-cadherin was stronger in MT intestinal than diffuse component (p < 0.05). Immunoreactivities to Ki-67, EMMPRIN, and VEGF were weaker in IT carcinoma than in the MT intestinal portion (p < 0.05), while the opposite was true for CD44, MUC-2, and MUC-6 (p < 0.05). The MT diffuse component displayed a higher expression of FHIT, VEGF, and P-GSK3β-ser9 than DT carcinoma (p < 0.05). The accumulative survival rate of the IT carcinoma patients was higher than the other types (p < 0.05). The invasive depth, venous invasion, lymph node, peritoneal or liver metastasis, and Lauren's classification were independent prognostic factors for gastric carcinomas (p < 0.05). These findings suggested that MT carcinomas were also indicated to be more aggressive than IT and DT carcinomas. Significant differences were observed in the proliferation, apoptosis, angiogenesis, mucin secretion, and cell adhesion between IT and DT carcinomas, whereas only a few of these characteristics showed differences between the MT intestinal and diffuse parts, thus suggesting that both the MT components might originate from the stem cells with similar genetic traits, but follow different histogenic pathways.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Oncotarget
                Journal ID (iso-abbrev): Oncotarget
                Journal ID (publisher-id): Oncotarget
                Journal ID (publisher-id): ImpactJ
                Title: Oncotarget
                Publisher: Impact Journals LLC
                ISSN (Electronic): 1949-2553
                Publication date Collection: 8 December 2017
                Publication date (Electronic): 3 November 2017
                Volume: 8
                Issue: 64
                Pages: 108261-108273
                Affiliations
                1 Department of Experimental Oncology and Animal Center, Shengjing Hospital of China Medical University, Shenyang 110004, China
                2 Department of Pathology, Harbin Medical University-Daqing, Daqing 163319, China
                Author notes
                Correspondence to: Hua-Chuan Zheng, zheng_huachuan@ 123456hotmail.com
                Article
                Publisher ID: 22369
                DOI: 10.18632/oncotarget.22369
                PMC ID: 5746141
                SO-VID: 0fdb982e-4b4e-4964-992b-2d5f3fd6f571
                Copyright © Copyright: © 2017 Zheng and Liu
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (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 : 1 August 2017
                Date accepted : 3 October 2017
                Categories
                Subject: Meta-Analysis

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: fhit,gastric cancer,meta-analysis,bioinformatics analysis
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: fhit, gastric cancer, meta-analysis, bioinformatics analysis

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