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      Meta-analysis of promoter methylation in eight tumor-suppressor genes and its association with the risk of thyroid cancer

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          Abstract

          Promoter methylation in a number of tumor-suppressor genes (TSGs) can play crucial roles in the development of thyroid carcinogenesis. The focus of the current meta-analysis was to determine the impact of promoter methylation of eight selected candidate TSGs on thyroid cancer and to identify the most important molecules in this carcinogenesis pathway. A comprehensive search was performed using Pub Med, Scopus, and ISI Web of Knowledge databases, and eligible studies were included. The methodological quality of the included studies was evaluated according to the Newcastle Ottawa scale table and pooled odds ratios (ORs); 95% confidence intervals (CIs) were used to estimate the strength of the associations with Stata 12.0 software. Egger’s and Begg’s tests were applied to detect publication bias, in addition to the “Metatrim” method. A total of 55 articles were selected, and 135 genes with altered promoter methylation were found. Finally, we included eight TSGs that were found in more than four studies ( RASSF1, TSHR, PTEN, SLC5A, DAPK, P16, RARβ2, and CDH1). The order of the pooled ORs for these eight TSGs from more to less significant was CDH1 (OR = 6.73), SLC5 (OR = 6.15), RASSF1 (OR = 4.16), PTEN (OR = 3.61), DAPK (OR = 3.51), P16 (OR = 3.31), TSHR (OR = 2.93), and RARβ2 (OR = 1.50). Analyses of publication bias and sensitivity confirmed that there was very little bias. Thus, our findings showed that CDH1 and SCL5A8 genes were associated with the risk of thyroid tumor genesis.

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          E-cadherin-integrin crosstalk in cancer invasion and metastasis.

          Marta Canel, Alan Serrels, Margaret Frame … (2013)
          E-cadherin is a single-pass transmembrane protein that mediates homophilic cell-cell interactions. Tumour progression is often associated with the loss of E-cadherin function and the transition to a more motile and invasive phenotype. This requires the coordinated regulation of both E-cadherin-mediated cell-cell adhesions and integrin-mediated adhesions that contact the surrounding extracellular matrix (ECM). Regulation of both types of adhesion is dynamic as cells respond to external cues from the tumour microenvironment that regulate polarity, directional migration and invasion. Here, we review the mechanisms by which tumour cells control the cross-regulation between dynamic E-cadherin-mediated cell-cell adhesions and integrin-mediated cell-matrix contacts, which govern the invasive and metastatic potential of tumours. In particular, we will discuss the role of the adhesion-linked kinases Src, focal adhesion kinase (FAK) and integrin-linked kinase (ILK), and the Rho family of GTPases.
          Article 0 comments Cited 261 times – based on 0 reviews     Review now
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            BRAF mutation in papillary thyroid cancer: pathogenic role, molecular bases, and clinical implications.

            Mingzhao Xing (2007)
            In recent years, the T1799A B-type Raf kinase (BRAF) mutation in thyroid cancer has received enthusiastic investigation, and significant progress has been made toward understanding its tumorigenic role and clinical significance. Among various thyroid tumors, this mutation occurs uniquely in papillary thyroid cancer (PTC), the most common endocrine malignancy, and some apparently PTC-derived anaplastic thyroid cancers. Many studies have found this mutation to be associated with those clinicopathological characteristics of PTC that are conventionally known to predict tumor progression and recurrence, including, for example, old patient age, extrathyroidal invasion, lymph node metastasis, and advanced tumor stages. Direct association of BRAF mutation with the clinical progression, recurrence, and treatment failure of PTC has also been demonstrated. The BRAF mutation has even been correlated with PTC recurrence in patients with conventionally low-risk clinicopathological factors. Some molecular mechanisms determining BRAF mutation-promoted progression and the aggressiveness of PTC have recently been uncovered. These include the down-regulation of major tumor suppressor genes and thyroid iodide-metabolizing genes and the up-regulation of cancer-promoting molecules, such as vascular endothelial growth factor, matrix metalloproteinases, nuclear transcription factor kappaB, and c-Met. Thus, BRAF mutation represents a novel indicator of the progression and aggressiveness of PTC. Significant advances have also occurred in the preclinical testing of new therapeutic strategies targeting the MAPK pathway aberrantly activated by BRAF mutation and other related mutations. New mitogen extracellular kinase (MEK) inhibitors developed recently are particularly promising therapeutic agents for thyroid cancer. With these advances, it has become clearer that BRAF mutation will likely have significant impact on the clinical management of PTC.
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              BRAF mutation predicts a poorer clinical prognosis for papillary thyroid cancer.

              Mingzhao Xing, William H Westra, Ralph P. Tufano … (2005)
              Use of BRAF mutation in papillary thyroid cancer (PTC) has the potential to improve risk stratification of this cancer. The objective of the study was to investigate the prognostic value of BRAF mutation in patients with PTC. In a multicenter study of 219 PTC patients, data on their clinicopathological characteristics and clinical courses between 1990 and 2004 were retrospectively collected, and their tumor BRAF mutation status was determined. Associations of BRAF mutation with initial tumor characteristics and subsequent recurrence were analyzed. Relationships between the BRAF mutation status and clinicopathological outcomes, including recurrence, were measured. We found a significant association between BRAF mutation and extrathyroidal invasion (P < 0.001), lymph node metastasis (P < 0.001), and advanced tumor stage III/IV (P = 0.007) at initial surgery. This association remained significant on multivariate analysis, adjusting for conventional clinicopathological predictors of recurrence excluding the histological PTC subtype, but was lost when the tumor subtype was included in the model. BRAF mutation was also significantly associated with tumor recurrence, 25 vs. 9% with and without mutation, respectively (P = 0.004), during a median of 15 (interquartile range, 3-29) months of follow-up. This association remained significant on multivariate analysis adjusting for conventional clinicopathological predictors of recurrence, even including the PTC subtype (odds ratio, 4.0; 95% confidence interval, 1.1-14.1; P = 0.03). BRAF mutation was even an independent predictor of recurrence in patients with stage I/II disease, 22 vs. 5% with and without BRAF mutation, respectively (P = 0.002). BRAF mutation was also more frequently associated with absence of tumor I-131 avidity and treatment failure of recurrent disease. In patients with PTC, BRAF mutation is associated with poorer clinicopathological outcomes and independently predicts recurrence. Therefore, BRAF mutation may be a useful molecular marker to assist in risk stratification for patients with PTC.
              Article 0 comments Cited 217 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Fatemeh Khatami:
                ORCID: http://orcid.org/0000-0002-6311-1336
                Role: Writing – original draft
                Bagher Larijani: Role: Supervision
                Ramin Heshmat: Role: Data curation
                Abbasali Keshtkar: Role: Data curationRole: Formal analysisRole: Methodology
                Mahsa Mohammadamoli: Role: Writing – review & editing
                Ladan Teimoori-Toolabi: Role: SoftwareRole: Visualization
                Shirzad Nasiri: Role: ResourcesRole: Validation
                Seyed Mohammad Tavangar:
                ORCID: http://orcid.org/0000-0002-4253-2385
                Role: ConceptualizationRole: InvestigationRole: SupervisionRole: Writing – review & editing
                Hiroyoshi Ariga: Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (iso-abbrev): PLoS ONE
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, CA USA )
                ISSN (Electronic): 1932-6203
                Publication date (Electronic): 19 September 2017
                Publication date Collection: 2017
                Volume: 12
                Issue: 9
                Electronic Location Identifier: e0184892
                Affiliations
                [1 ] Chronic Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran
                [2 ] Endocrinology and Metabolism Research Center, Endocrinology and Metabolism Clinical Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran
                [3 ] Department of Health Sciences Education Development, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
                [4 ] Molecular Medicine Department, Pasteur Institute of Iran, Tehran, Iran
                [5 ] Department of Surgery, Tehran University of Medical Sciences, Shariati Hospital, Tehran, Iran
                [6 ] Department of Pathology, Dr. Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran
                Hokkaido Daigaku, JAPAN
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                ‡ These authors also contributed equally to this work

                Author information
                http://orcid.org/0000-0002-6311-1336
                http://orcid.org/0000-0002-4253-2385
                Article
                Publisher ID: PONE-D-17-23998
                DOI: 10.1371/journal.pone.0184892
                PMC ID: 5605048
                PubMed ID: 28926589
                SO-VID: d6dc9db7-81a0-403a-bc07-0691b2b3e9ba
                Copyright © © 2017 Khatami et al
                License:

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

                History
                Date received : 24 June 2017
                Date accepted : 3 September 2017
                Page count
                Figures: 4, Tables: 0, Pages: 16
                Funding
                The authors received no specific funding for this work.
                Categories
                Subject: Research Article
                Subject: Medicine and Health Sciences
                Subject: Oncology
                Subject: Cancers and Neoplasms
                Subject: Lung and Intrathoracic Tumors
                Subject: Thymic Tumors
                Subject: Thyroid Carcinomas
                Subject: Medicine and Health Sciences
                Subject: Oncology
                Subject: Cancers and Neoplasms
                Subject: Carcinomas
                Subject: Thyroid Carcinomas
                Subject: Medicine and Health Sciences
                Subject: Oncology
                Subject: Cancers and Neoplasms
                Subject: Endocrine Tumors
                Subject: Thyroid Carcinomas
                Subject: Physical Sciences
                Subject: Chemistry
                Subject: Chemical Reactions
                Subject: Methylation
                Subject: Research and Analysis Methods
                Subject: Mathematical and Statistical Techniques
                Subject: Statistical Methods
                Subject: Meta-Analysis
                Subject: Physical Sciences
                Subject: Mathematics
                Subject: Statistics (Mathematics)
                Subject: Statistical Methods
                Subject: Meta-Analysis
                Subject: Biology and Life Sciences
                Subject: Anatomy
                Subject: Endocrine System
                Subject: Thyroid
                Subject: Medicine and Health Sciences
                Subject: Anatomy
                Subject: Endocrine System
                Subject: Thyroid
                Subject: Science Policy
                Subject: Research Integrity
                Subject: Publication Ethics
                Subject: Biology and life sciences
                Subject: Cell biology
                Subject: Chromosome biology
                Subject: Chromatin
                Subject: Chromatin modification
                Subject: DNA methylation
                Subject: Biology and life sciences
                Subject: Genetics
                Subject: Epigenetics
                Subject: Chromatin
                Subject: Chromatin modification
                Subject: DNA methylation
                Subject: Biology and life sciences
                Subject: Genetics
                Subject: Gene expression
                Subject: Chromatin
                Subject: Chromatin modification
                Subject: DNA methylation
                Subject: Biology and life sciences
                Subject: Genetics
                Subject: DNA
                Subject: DNA modification
                Subject: DNA methylation
                Subject: Biology and life sciences
                Subject: Biochemistry
                Subject: Nucleic acids
                Subject: DNA
                Subject: DNA modification
                Subject: DNA methylation
                Subject: Biology and life sciences
                Subject: Genetics
                Subject: Epigenetics
                Subject: DNA modification
                Subject: DNA methylation
                Subject: Biology and life sciences
                Subject: Genetics
                Subject: Gene expression
                Subject: DNA modification
                Subject: DNA methylation
                Subject: Biology and Life Sciences
                Subject: Genetics
                Subject: Epigenetics
                Subject: Medicine and Health Sciences
                Subject: Oncology
                Subject: Carcinogenesis
                Custom metadata
                Data Availability All relevant data are within the paper and its Supporting Information files.

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