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      SATB1 Expression Is Associated with Biologic Behavior in Colorectal Carcinoma In Vitro and In Vivo

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          Abstract

          There is increasing evidence that Special AT-rich sequence-binding protein 1 (SATB1) is aberrantly expressed in several cancers and is correlated with clinicopathologic parameters in these tumors. In this study, we showed over-expression of SATB1 in 80 cases of colorectal cancer and in 3 colorectal cancer cell lines and found expression levels were strongly associated with tumor differentiation and stage. Expression levels of SATB1 protein were higher in poorly-differentiated as compared with well-differentiated cell lines, and both quantity and distribution patterns of SATB1 were associated with tumor differentiation and pTNM stage. Strikingly, we further investigated the effect of down regulation of SATB1 expression on malignant phenotypic features in colorectal cancer cells in vitro, and showed that SABT1 down-regulation negatively affected growth potential, anchorage-independent colony formation and cancer cell invasion, and resulted in increased apoptosis. SATB1 expression was positively associated with the expression of various biological and genetic markers, including Cyclin D1, MMP-2, NF-κB, and PCNA, and was associated with loss of APC and BRAF V600E. These findings suggest that SATB1 is involved in the carcinogenesis, development and progression of colorectal cancer.

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          BRAF mutation is associated with DNA methylation in serrated polyps and cancers of the colorectum.

          Takeshi Kambara, Ellen L Simms, V Whitehall … (2004)
          Mutations in BRAF have been linked with colorectal cancers (CRC) showing high level microsatellite instability (MSI-H). However, the distribution of BRAF mutations in MSI-H cancers remains to be clarified with respect to precursor lesions and the CpG island methylator phenotype (CIMP). Forty three hyperplastic polyps (HP), nine mixed polyps (MP), five serrated adenomas (SA), 28 conventional adenomas (AD), 18 hereditary non-polyposis colorectal cancers (HNPCC), and 127 sporadic CRC (46 MSI-H and 81 non-MSI-H) were collected from patients undergoing colectomy for either CRC or hyperplastic polyposis. Twenty five of 57 serrated lesions were derived from four patients with hyperplastic polyposis. HP were further subdivided according to recently documented morphological criteria into 27 classical HP and 16 variant lesions described as "sessile serrated adenoma" (SSA). All tumours were screened for BRAF activating mutations. The BRAF mutation was more frequent in SSA (75%) and MP (89%) than in classical HP (19%), SA (20%), and AD (0%) (p<0.0001), and also in sporadic MSI-H cancers (76%) compared with HNPCC (0%) and sporadic non-MSI-H cancers (9%) (p<0.0001). The BRAF mutation was identified more often in CIMP-high serrated polyps (72%) and CIMP-high CRC (77%) than in CIMP-low (30%) and CIMP-negative (13%) polyps (p = 0.002) as well as CIMP-low (18%) and CIMP-negative (0%) CRC (p<0.0001). The BRAF mutation was frequently seen in SSA and in sporadic MSI-H CRC, both of which were associated with DNA methylation. Sporadic MSI-H cancers may originate in SSA and not adenomas, and BRAF mutation and DNA methylation are early events in this "serrated" pathway.
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            Correlation of tumour BRAF mutations and MLH1 methylation with germline mismatch repair (MMR) gene mutation status: a literature review assessing utility of tumour features for MMR variant classification.

            Michael Parsons, Daniel D. Buchanan, Bryony Thompson … (2012)
            Colorectal cancer (CRC) that demonstrates microsatellite instability (MSI) is caused by either germline mismatch repair (MMR) gene mutations, or 'sporadic' somatic tumour MLH1 promoter methylation. MLH1 promoter methylation is reportedly correlated with tumour BRAF V600E mutation status. No systematic review has been undertaken to assess the value of BRAF V600E mutation and MLH1 promoter methylation tumour markers as negative predictors of germline MMR mutation status. A literature review of CRC cohorts tested for MMR mutations, and tumour BRAF V600E mutation and/or MLH1 promoter methylation was conducted using PubMed. Studies were assessed for tumour features, stratified by tumour MMR status based on immunohistochemistry or MSI where possible. Pooled frequencies and 95% CIs were calculated using a random effects model. BRAF V600E results for 4562 tumours from 35 studies, and MLH1 promoter methylation results for 2975 tumours from 43 studies, were assessed. In 550 MMR mutation carriers, the BRAF V600E mutation frequency was 1.40% (95% CI 0.06% to 3%). In MMR mutation-negative cases, the BRAF V600E mutation frequency was 5.00% (95% CI 4% to 7%) in 1623 microsatellite stable (MSS) cases and 63.50% (95% CI 47% to 79%) in 332 cases demonstrating MLH1 methylation or MLH1 expression loss. MLH1 promoter methylation of the 'A region' was reported more frequently than the 'C region' in MSS CRCs (17% vs 0.06%, p<0.0001) and in MLH1 mutation carriers (42% vs 6%, p<0.0001), but not in MMR mutation-negative MSI-H CRCs (40% vs 47%, p=0.12). Methylation of the 'C region' was a predictor of MMR mutation-negative status in MSI-H CRC cases (47% vs 6% in MLH1 mutation carriers, p<0.0001). This review demonstrates that tumour BRAF V600E mutation, and MLH1 promoter 'C region' methylation specifically, are strong predictors of negative MMR mutation status. It is important to incorporate these features in multifactorial models aimed at predicting MMR mutation status.
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              Human epithelial cancers secrete immunoglobulin g with unidentified specificity to promote growth and survival of tumor cells.

              Peng Lv, Jie Zheng, Chunmei Hou … (2003)
              Immunoglobulins (Igs) are found thus far only to be produced by differentiated B lymphocytes. By immunohistochemistry analysis, in situ hybridization, and laser capture microdissection-assisted single-cell PCR, we demonstrate that human cancers of epithelial origin, including carcinomas of breast, colon, liver, lung, established epithelial cancer lines, as well as some normal lung tissues, also produce IgG in both cytoplasmic and secreted forms. Furthermore, blockade of tumor-derived IgG by either antisense DNA or antihuman IgG antibody increased programmed cell death and inhibited growth of cancer cells in vitro. More importantly, administration of antihuman IgG antibody also suppressed the growth of an IgG-secreting carcinoma line in immunodeficient nude mice. Our results support a role of tumor-derived IgG as growth factor for epithelial cancers. Prevalent expression of IgG in human carcinomas and its growth-promoting functions may have important implications in growth regulation and targeted therapy of human cancers.
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                Author and article information

                Contributors
                Ramon Andrade de Mello: 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, USA )
                ISSN (Electronic): 1932-6203
                Publication date Collection: 2013
                Publication date (Electronic): 11 January 2013
                Volume: 8
                Issue: 1
                Electronic Location Identifier: e47902
                Affiliations
                [1 ]Department of Human Anatomy, Weifang Medical University, Weifang, China
                [2 ]Department of Pathology, Weifang Medical University, Weifang, China
                [3 ]Department of Pathology, affiliated hospital of Weifang Medical University, Weifang, China
                [4 ]Department of Anesthesia, Weifang Medical University, Weifang, China
                [5 ]Department of Pathology, Cancer hospital of Shantou University Medical College, Shantou, China
                [6 ]Department of Pathology, School of Basic Medical Sciences, Peking University, Beijing, China
                [7 ]Department of Clinical Laboratory, Peking Union Medical College Hospital and Peking Union Medical College, Beijing, China
                [8 ]Department of Neurology, Weifang Medical University, Weifang, China
                [9 ]Key Laboratory for Immunology in Universities of Shandong Province, Weifang Medical University, Weifang, China
                University of Porto, Portugal
                Author notes

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

                Conceived and designed the experiments: BZ NN. Analyzed the data: BZ NN ZL XW. Acquisition of data: JZ YS NN SL YL MW XZ. Drafting of the manuscript: MM NN DZ. Approval of the final version of this manuscript: JZ BZ XZ YS XW MM SL YL DZ MW ZL NN.

                Article
                Publisher ID: PONE-D-12-15004
                DOI: 10.1371/journal.pone.0047902
                PMC ID: 3543436
                PubMed ID: 23326301
                SO-VID: c9ceb506-588d-4b4e-ab74-9c472089dec7
                Copyright statement: Copyright @ 2013
                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 : 25 May 2012
                Date accepted : 18 September 2012
                Page count
                Pages: 8
                Funding
                This work was supported by grants from the Young and Middle-Aged Scientists Research Awards Fundation of Shandong Province to Na Niu (No. BS2011SW051) and Baogang Zhang (No.2010BSB14050), and National Natural Science Foundation of China to Na Niu (No.81100885) and Baogang Zhang (No.81072068). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Subject: Research Article
                Subject: Biology
                Subject: Developmental Biology
                Subject: Cell Differentiation
                Subject: Medicine
                Subject: Diagnostic Medicine
                Subject: Pathology
                Subject: General Pathology
                Subject: Biomarkers
                Subject: Gastroenterology and Hepatology
                Subject: Gastrointestinal Cancers
                Subject: Oncology
                Subject: Basic Cancer Research
                Subject: Tumor Physiology
                Subject: Cancer Risk Factors
                Subject: Genetic Causes of Cancer
                Subject: Cancers and Neoplasms
                Subject: Gastrointestinal Tumors
                Subject: Colon Adenocarcinoma
                Subject: Rectal Cancer

                ScienceOpen disciplines: Uncategorized
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                ScienceOpen disciplines: Uncategorized

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