Frequent overexpression of CADM1/IGSF4 in lung adenocarcinoma

Kitamura, Yuka; Kurosawa, Gene; Tanaka, Miho; Sumitomo, Mariko; Muramatsu, Chiho; Eguchi, Kaoru; Akahori, Yasushi; Iba, Yoshitaka; Tsuda, Hiroyuki; Sugiura, M.; Hattori, Yoshinobu; Kurosawa, Yoshikazu

doi:10.1016/j.bbrc.2009.04.039

Cited by 10 publications

(6 citation statements)

References 21 publications

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“…However, it would be difficult to determine the precise location of CADM1/TSLC1 in Figure 3, and Kitamura et al . reported that CADM1/TSLC1 was distributed not only in cytoplasm but also on surface of lung adenocarcinoma cells, which was revealed by immunohistochemical analysis with 8 monoclonal antibodies 18. It could be caused by the epitope specificity of different antibodies.…”

Section: Discussionmentioning

confidence: 98%

CADM1/TSLC1 inactivation by promoter hypermethylation is a frequent event in colorectal carcinogenesis and correlates with late stages of the disease

Chen

Wang

Peng

et al. 2010

Intl Journal of Cancer

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Cell adhesion molecule 1 (CADM1/TSLC1), a putative tumor suppressor involving in cell adhesion, proliferation and apoptosis, is frequently inactivated in several carcinomas due to promoter hypermethylation. But alterations of CADM1/TSLC1 in colorectal carcinogenesis and clinical significance have not been elucidated yet. The aim of this study was to determine the role of functional inactivation of CADM1/TSLC1 gene in colorectal tumorigenesis and its potential as a novel epigenetic marker for clinical assessment of patients with colorectal cancer. We measured CADM1/TSLC1 expression levels in 8 colorectal cancer cell lines, 54 primary colorectal carcinomas and their corresponding non-cancerous tissues by reverse transcription polymerase chain reaction, western blot analysis and immunohistochemistry. We analyzed CADM1/TSLC1 promoter methylation status by bisulfite genomic sequencing and the methylation special polymerase chain reaction, and evaluated its correlation with clinicopathological characteristics. All statistical tests were 2-sides. Downregulation of CADM1/ TSLC1 expression was observed in 7 of 8 (88%) colorectal cancer cell lines and in 39 of 54 (72%) primary colorectal carcinomas. Hypermethylation of CADM1/TSLC1 promoter region occurred in 6 of 8 (75%) colorectal cancer cell lines and 32 of 54 (59%) primary colorectal carcinomas, and was correlated with advanced colorectal carcinoma. Epigenetic inactivation of CADM1/TSLC1 gene is a frequent alteration in development of colorectal cancer and can be a potential biomarker for molecular staging of patients with colorectal cancer.Colorectal carcinoma is one of the most common malignancies, which is attributable much to the inactivation of tumor suppressor genes (TSGs). Besides gene mutations and deletions, DNA methylation of CpG islands in the promoter of TSGs is a major mechanism underlying TSGs inactivation. Lots of studies have shown that the promoter hypermethylation of many TSGs, such as MLH1, P16, TIMP3 and P14, is associated with colorectal carcinoma. 1 A recent study further showed that promoter hypermethylation of methylguanine DNA methyltransferase, human Mut L homolog-1 and vimentin in stool samples could be used as a feasible epigenetic biomarker for colorectal carcinoma screening. 2 Thus, promoter methylation of TSGs could serve as potential diagnostic, therapeutic and prognostic targets for colorectal carcinoma.

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Section: Discussionmentioning

confidence: 98%

CADM1/TSLC1 inactivation by promoter hypermethylation is a frequent event in colorectal carcinogenesis and correlates with late stages of the disease

Chen

Wang

Peng

et al. 2010

Intl Journal of Cancer

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“…Inactivation of the TSLC1 gene, which leads to the suppression of Necl-2 expression, has been frequently described in various human cancers, including lung, cervical, and breast cancers (38). Conversely, Necl-2 was found to be expressed de novo in adult T leukemia or overexpressed in certain other tumors (39)(40)(41)(42)(43). Thus, similar to tumor-associated molecules, such as FasL or PD-L1, Necl-2 in tumor cells may represent a new tumor counterattack mechanism to evade immunosurveillance by Vg9Vd2 T cells (44).…”

Section: Discussionmentioning

confidence: 99%

CRTAM Receptor Engagement by Necl-2 on Tumor Cells Triggers Cell Death of Activated Vγ9Vδ2 T Cells

Dessarthe

Thedrez

Latouche

et al. 2013

The Journal of Immunology

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Human Vγ9Vδ2 T cells exert potent in vitro and in vivo antitumor activities, making them promising candidates for immunotherapy strategies. Recognition of tumor cells by Vγ9Vδ2 T cells requires engagement of the TCR and/or NK receptors. Recently, one of the novel NK receptors, the class I–restricted T cell–associated molecule (CRTAM), has been described to promote cytotoxic function of NK cells and to lead to IFN-γ secretion by CD8+ T cells through interaction with its ligand, Necl-2. A better understanding of the role of CRTAM in Vγ9Vδ2 T cell functions is highly relevant to optimize innate-like T cell–based cancer immunotherapy. In this article, we report that CRTAM is transiently expressed on activated Vγ9Vδ2 T lymphocytes following TCR engagement. However, CRTAM–Necl-2 interaction does not modify the cytotoxic function or IFN-γ secretion of Vγ9Vδ2 T cells. The expression of CRTAM in activated Vγ9Vδ2 T cells is quickly downregulated following interaction with Necl-2 on tumor cells. Of interest, CRTAM is concurrently acquired at the cell surface of Necl-2+ tumor cells through Vγ9Vδ2 T cell membrane capture. Finally, we highlight that coculture experiments with tumor cells expressing Necl-2 result in significant cell death of CRTAM+ Vγ9Vδ2 T cells. CRTAM-mediated cell death is dependent on an autophagic process, but not on apoptosis or necroptosis, as attested by the expression of characteristic markers and blocking experiments with specific inhibitors. On the basis of these findings, we propose that Necl-2 on tumor cells represents a new tumor counterattack mechanism and a potential target to improve efficiency of γδ T cell–based immunotherapy.

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“…The salient feature of this ICOS method exists in the washing procedure using organic solvent mixtures, thereby allowing the antibodies against the epitopes actually present on the cell surface to be obtained with high efficiency. ( 4–6,16 ) Twenty‐nine TAA have been identified to date. Regarding adverse side‐effects, the target Ag should not be highly expressed on normal cells, especially those that constitute vital organs.…”

Section: Discussionmentioning

confidence: 99%

“…(2009). ( 16 ) Each tissue specimen was processed following these procedures: cut into pieces, de‐aired, fixated, washed and embedded. The specimen was then stored at −80°C.…”

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confidence: 99%

Selection and analysis of anti‐cancer antibodies for cancer therapy obtained from antibody phage library

et al. 2010

Self Cite

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The search for effective antibodies (Ab) for curable cancer immunotherapy has been a quest of many research groups in order to find an effective target that exists on the cancer cell surface. So far there have been no conclusive answers to shed light on the search. This study therefore aimed to bridge the gap of cancer therapy. Screening against 49 kinds of cell lines belonging to 11 kinds of solids cancers was performed. Isolation and characterization for approximately 4200 monoclonal antibodies (mAb) was also performed thereafter. Of those mAb 488 clones that turned out to bind to 29 tumor-associated antigens (TAA) were subjected to immunohistochemical (IHC) analyses. Selection of target antigens (Ag) and a potential antibody for cancer therapy was conducted prior to clinical examinations. In order to find predictably effective targets for therapeutic Ab against solid cancers, expression of the Ag on the surface of cancer and normal cells was extensively examined by IHC analyses using fresh cancer specimens resected from patients. In this study, the tendencies of all staining patterns and distribution of the Ab are reported. While all of the TAA appeared to be involved in tumorigenesis, their expression was not restricted to some specific tumor types but rather randomly distributed among various cancers. Some kinds of Ab including anti-epidermal growth factor receptor (EGFR) and anti-human epidermal growth factor receptor 2 (HER2) indicated the frequency of expression in normal cells was generally low. We concluded that identification of 488 mAb and the accumulated results of IHC analyses in this study could be the key for further therapeutic Ab against cancers. The targets that showed cancer-specific expression are expected to be better for therapeutic Ab than the other Ab. Moreover, further investigation into the growth of cancer cell lines using full human IgG form of Ab shows available efficacy in specific cases. (Cancer Sci 2011; 102: 175-181)

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Frequent overexpression of CADM1/IGSF4 in lung adenocarcinoma

Cited by 10 publications

References 21 publications

CADM1/TSLC1 inactivation by promoter hypermethylation is a frequent event in colorectal carcinogenesis and correlates with late stages of the disease

CADM1/TSLC1 inactivation by promoter hypermethylation is a frequent event in colorectal carcinogenesis and correlates with late stages of the disease

CRTAM Receptor Engagement by Necl-2 on Tumor Cells Triggers Cell Death of Activated Vγ9Vδ2 T Cells

Selection and analysis of anti‐cancer antibodies for cancer therapy obtained from antibody phage library

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