A 2-Mb Sequence-Ready Contig Map and a Novel Immunoglobulin Superfamily Gene IGSF4 in the LOH Region of Chromosome 11q23.2

Gomyo, Hiroki; Arai, Yasuhito; Tanigami, Akira; Murakami, Yoshinori; Hattori, Masahira; Hosoda, Fumie; Arai, Kyoko; Aikawa, Yuri; Tsuda, Hitoshi; Hirohashi, Setsuo; Asakawa, Shuichi; Shimizu, Nobuyoshi; Soeda, Eiichi; Sakaki, Yoshiyuki; Ohki, Masafumi

doi:10.1006/geno.1999.6001

Cited by 99 publications

(78 citation statements)

References 26 publications

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“…Differential expression of a number of transcripts was confirmed by quantitative real-time RT-PCR in these stages, including the putative tumour suppressor gene cell adhesion molecule 1 (CADM1), which is also known as TSLC1, IGSF4, SynCAM and Necl-2 (Fischer et al, 2006). This gene maps to chromosome 11q23.2, a region frequently deleted in tumours such as malignant melanoma (Katoh, 2003(Katoh, , 2004, lung cancer (Gomyo et al, 1999) and neuroblastoma (Mertens et al, 1997), and encodes an immunoglobulin superfamily transmembrane molecule primarily involved in epithelial cell adhesion (Murakami, 2005). Loss of CADM1 expression has been described in many malignancies, including liver, pancreatic, breast, brain and prostate cancers, particularly in those showing invasion or metastasis (Kuramochi et al, 2001;Fukuhara et al, 2002;Jansen et al, 2002;Houshmandi et al, 2006;Heller et al, 2007).…”

Section: Introductionmentioning

confidence: 94%

Expression of the tumour suppressor gene CADM1 is associated with favourable outcome and inhibits cell survival in neuroblastoma

et al. 2007

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Section: Introductionmentioning

confidence: 94%

Expression of the tumour suppressor gene CADM1 is associated with favourable outcome and inhibits cell survival in neuroblastoma

et al. 2007

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“…These findings suggest that the disruption of TSLC1 function would participate in the invasion or metastasis of human tumors. Recently, TSLC1 was found to play specific roles in cell adhesion of various tissues in addition to epithelium and has been termed TSLC1/IGSF4/RA175/Necl2/SgIGSF/SynCAM1 (Gomyo et al, 1999;Kuramochi et al, 2001;Wakayama et al, 2001;Biederer et al, 2002;Fujita et al, 2003;Shingai et al, 2003;Murakami, 2005).…”

Section: Introductionmentioning

confidence: 99%

Cell adhesion and prostate tumor-suppressor activity of TSLL2/IGSF4C, an immunoglobulin superfamily molecule homologous to TSLC1/IGSF4

Williams

Masuda²,

Sakurai-Yageta³

et al. 2005

Oncogene

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The TSLL2/IGSF4C encodes an immunoglobulin (Ig) superfamily molecule showing significant homology with a lung tumor suppressor, TSLC1. The TSLL2 protein of 55 kDa is mainly expressed in the kidney, bladder, and prostate in addition to the brain. Here, we report the biological significance of TSLL2 in the urinary tissues. An immunohistochemical study reveals that TSLL2 is expressed at the cell-cell attachment sites in the renal tubules, the transitional epithelia of the bladder, and the glandular epithelia of the prostate. Confocal microscopy analysis demonstrates that TSLL2 is localized in the lateral membranes in polarized Mardin-Darby canine kidney (MDCK) cells. TSLL2 forms homo-dimers and its overexpression induces aggregation of suspended MDCK cells in a Ca 2 þ /Mg 2 þ -independent manner, suggesting that it is involved in cell adhesion through homophilic trans-interaction. The TSLL2 gene is mapped on the chromosomal region 19q13.2, whose loss of heterozygosity has been frequently reported in prostate cancer. TSLL2 protein is lost in nine of nine primary prostate cancers and in a prostate cancer cell, PPC-1. Introduction of TSLL2 into PPC-1 strongly suppresses subcutaneous tumor formation in nude mice. These results suggest that TSLL2 is a new member of the Ig superfamily cell adhesion molecules and is a tumor-suppressor candidate in prostate cancer.

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“…Necl-2 is known by many names: IgSF4a, RA175, SgIGSF, TSLC1, and SynCAM1 (15)(16)(17)(18)(19). Necl-2 was directly reported in GenBank TM in 1998; IgSF4a was identified as a candidate for a tumor suppressor gene in the loss of heterozygosity region of chromosome 11q23.2 (16); RA175 was identified as a gene highly expressed during the neuronal differentiation of embryonic carcinoma cells (19); SgIGSF was identified as a gene expressed in spermatogenic cells during the early stages of spermatogenesis (18); TSLC1 was identified as a tumor suppressor in human non-small cell lung cancer (17); and SynCAM1 was identified as a brain-specific synaptic adhesion molecule (15).…”

mentioning

confidence: 99%

Silencing of ErbB3/ErbB2 Signaling by Immunoglobulin-like Necl-2

Kawano

Ikeda²,

Kishimoto

et al. 2009

Journal of Biological Chemistry

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ErbB2 and ErbB3, members of the EGF receptor/ErbB family, form a heterodimer upon binding of a ligand, inducing the activation of Rac small G protein and Akt protein kinase for cell movement and survival, respectively. The enhanced ErbB3/ ErbB2 signaling causes tumorigenesis, invasion, and metastasis. We found here that the ErbB3/ErbB2 signaling is regulated by immunoglobulin-like Necl-2, which is down-regulated in various cancer cells and serves as a tumor suppressor. The extracellular region of ErbB3, but not ErbB2, interacted in cis with that of Necl-2. This interaction reduced the ligand-induced, ErbB2-catalyzed tyrosine phosphorylation of ErbB3 and inhibited the consequent ErbB3-mediated activation of Rac and Akt, resulting in the inhibition of cancer cell movement and survival. These inhibitory effects of Necl-2 were mediated by the protein-tyrosine phosphatase PTPN13 which interacted with the cytoplasmic tail of Necl-2. We describe here this novel mechanism for silencing of the ErbB3/ErbB2 signaling by Necl-2.ErbB2 and ErbB3 are members of the EGF receptor/ErbB family, which has ErbB1 and ErbB4 as additional members (1). ErbB2 and ErbB3 are also known as HER2/Neu and HER3, respectively. No ligands binding directly to ErbB2 have been identified yet, whereas heregulin (HRG) 3 -␣ and -␤, also known as neuregulin-1 and -2, respectively, directly bind to ErbB3. ErbB2 and ErbB3 have kinase domains in their cytoplasmic tails, but that of ErbB3 lacks kinase activity. Therefore, the homodimer of ErbB3 formed by binding of HRG does not transduce any intracellular signaling. By contrast, ErbB2 heterophilically interacts in cis with HRG-occupied ErbB3 and phosphorylates nine tyrosine residues of ErbB3, causing recruitment and activation of the p85 subunit of phosphoinositide 3-kinase (PI3K) and the subsequent activation of Rac small G protein and Akt protein kinase (2). The activation of Rac enhances cell movement and that of Akt prevents cell apoptosis (3).ErbB2 serves as an oncogenic protein (4), and amplification of the ErbB2 gene is observed in many types of cancers. For instance, it is amplified in ϳ3% of lung cancers, ϳ30% of breast cancers, ϳ20% of gastric cancers, and ϳ60% of ovarian cancers (5). Moreover, mutation of the ErbB2 gene is found in many types of cancers, namely, ϳ10% of lung cancers, ϳ4% of breast cancers, ϳ5% of gastric cancers, and ϳ3% of colorectal cancers (6). This gene amplification or mutation causes enhanced signaling for cell movement and survival, eventually resulting in tumorigenesis, invasiveness, and metastasis. On the basis of these properties of ErbB2, it has been recognized as a good target for cancer therapy; indeed, ErbB2-targeting drugs have already been developed and used clinically (7,8). However, it remains unknown whether ErbB2 is involved in oncogenesis in cancers in which its gene is not amplified or mutated. In addition, it was recently reported that overexpression of ErbB3 is also involved in tumor malignancy (9), but it remains unknown how ErbB3 serves as an oncogenic p...

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A 2-Mb Sequence-Ready Contig Map and a Novel Immunoglobulin Superfamily Gene IGSF4 in the LOH Region of Chromosome 11q23.2

Cited by 99 publications

References 26 publications

Expression of the tumour suppressor gene CADM1 is associated with favourable outcome and inhibits cell survival in neuroblastoma

Expression of the tumour suppressor gene CADM1 is associated with favourable outcome and inhibits cell survival in neuroblastoma

Cell adhesion and prostate tumor-suppressor activity of TSLL2/IGSF4C, an immunoglobulin superfamily molecule homologous to TSLC1/IGSF4

Silencing of ErbB3/ErbB2 Signaling by Immunoglobulin-like Necl-2

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