Rapid divergency of rodent CD99 orthologs: Implications for the evolution of the pseudoautosomal region

Park, Seong Hoe; Shin, Young Kee; Suh, Young Ho; Park, Won Seo; Ban, Young Larn; Choi, Hueng-Sik; Park, Hyojin; Jung, Kyeong Cheon

doi:10.1016/j.gene.2005.04.023

Cited by 31 publications

(50 citation statements)

References 28 publications

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“…12 and unpublished observation). Additionally, activated mouse T cells express CD99 (13), which is recognized by PILR␣-Ig (Fig. 6).…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, the activating PILR␤ seems to be involved in target cell recognition by NK cells. Furthermore, analysis using an anti-CD99 mAb indicated that CD99 is highly expressed on activated T cells (13). Because PILR␣ and PILR␤ are expressed on dendritic cells (9,12), interaction between CD99 and PILR might be involved in the regulation of dendritic cell function by T cells.…”

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confidence: 99%

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An Essential Role of Sialylated O-Linked Sugar Chains in the Recognition of Mouse CD99 by Paired Ig-Like Type 2 Receptor (PILR)

Wang

Shiratori

Satoh

et al. 2008

The Journal of Immunology

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The paired Ig-like type 2 receptor (PILR), which comprises both inhibitory and activating isoforms, is well conserved among most mammalians. The inhibitory PILRα possesses an ITIM in its cytoplasmic domain, whereas the activating PILRβ does not have an ITIM but transduces activating signals by associating with the ITAM-bearing DAP12 adapter molecule. Both mouse PILRα and PILRβ recognize mouse CD99, which is broadly expressed on various cells, including lymphocytes, and is involved in the regulation of immune responses. We herein report that sialylated O-linked sugar chains on CD99 are essential for the recognition by PILR. Mutations of one of two O-glycosylation sites on CD99 significantly reduced recognition of CD99 by the activating PILRβ, whereas recognition by the inhibitory PILRα was not affected. In contrast, mutations of both O-glycosylation sites on CD99 completely abrogated the recognition by both PILRα and PILRβ. PILR did not recognize CD99 treated with neuraminidase, and CD99 expressed on cells transfected with core 2 β-1,6-N-acetylglucosaminyltransferase was not recognized by PILR. NK cells expressing endogenous activating PILRβ receptors mediated cytotoxicity against cells expressing wild-type CD99 but not cells expressing mutant CD99 that lacked O-glycosylation sites. These findings indicate that sialylated O-linked sugar structures on CD99 play an important role in the recognition of PILR.

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“…12 and unpublished observation). Additionally, activated mouse T cells express CD99 (13), which is recognized by PILR␣-Ig (Fig. 6).…”

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

An Essential Role of Sialylated O-Linked Sugar Chains in the Recognition of Mouse CD99 by Paired Ig-Like Type 2 Receptor (PILR)

Wang

Shiratori

Satoh

et al. 2008

The Journal of Immunology

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“…It has also been shown that the CD99 down-regulation leads to the loss of normal morphology in Hodgkin's disease (13,17). Fourth, because the mouse CD99 orthologue has been found to specifically activate natural killer cells and dendritic cells by binding to PILRB (33,34), the loss of CD99 in gastric carcinoma may serve as an immune escape mechanism.…”

Section: Discussionmentioning

confidence: 99%

Clinical Significance of CD99 Down-Regulation in Gastric Adenocarcinoma

Lee

Kim

Wang

et al. 2007

Clinical Cancer Research

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Purpose: CD99 is a cell adhesion molecule associated with human tumors. The aim of the present study was to characterize its role in the development and progression of human gastric adenocarcinoma. Experimental Design: The expression of CD99 was investigated in 283 gastric adenocarcinomas and related lesions and 9 gastric carcinoma cell lines.We also analyzed the methylation status of CD99 gene by using methylation-specific PCR and examined loss of heterozygosity (LOH) of this gene locus by using an intragenic marker. Moreover, we assessed whether SP1, a positive transcription factor for CD99, is expressed in these samples. Results: We found that the decreased expression of CD99 was strongly associated with poor survival and unfavorable clinicopathologic variables. Promoter region methylation (15 of 89, 16.9%) and LOH (21 of 74, 28.4%) were observed and significantly associated with CD99 down-regulation (P < 0.05). In addition, most of the gastric adenocarcinoma cases with CD99 down-regulation had reduced expression of SP1 (47 of 103, 45.6%; P < 0.01). This relationship between CD99 and SP1was consolidated by using SP1small interfering RNA transfection experiment and CD99 promoter luciferase assay. Furthermore, we showed that CD99 down-regulation was associated with proliferation and migration in gastric carcinoma cell line. Conclusion: These observations suggest that CD99 down-regulation is a critical event in the progression of gastric adenocarcinoma, and CD99 promoter methylation, CD99 LOH, and SP1 down-regulation were responsible for the down-regulation of CD99.

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“…With the exception of lymphoblastic lymphoma, ESFT remain the only class of tumors that most consistently expresses CD99, a feature widely employed in the differential diagnosis of ESFT among small-round-cell tumors of childhood (Fellinger et al, 1991). CD99 shares no structural homology with any known protein family and putative rodent orthologs significantly diverge from human CD99 (Park et al, 2005). Available functional data on CD99 derive from triggering CD99 by agonistic monoclonal antibodies.…”

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confidence: 99%

Suppression of KCMF1 by constitutive high CD99 expression is involved in the migratory ability of Ewing's sarcoma cells

et al. 2005

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High CD99 expression levels and rearrangements of the EWS gene with ETS transcription factor genes characterize the Ewing's sarcoma family of tumors (ESFT). CD99 is a cell surface glycoprotein whose engagement has been implicated in cell proliferation as well as upregulation and transport of several transmembrane proteins in hematopoietic cells. In ESFT, antibody ligation of CD99 induces fast homotypic cell aggregation and cell death although its functional role in these processes remains largely unknown. Here, using an RNAi approach, we studied for the first time the consequences of modulated CD99 expression in six different ESFT cell lines, representing the most frequent variant forms of EWS gene rearrangement. CD99 suppression resulted in growth inhibition and reduced migration of ESFT cells. Among genes whose expression changes in response to CD99 modulation, the potassium-channel modulatory factor KCMF1 was consistently upregulated. In a series of 22 primary ESFT, KCMF1 expression levels inversely correlated with CD99 abundancy. Cells forced to express ectopic KCMF1 showed a similar reduction in migratory ability as CD99 silenced ESFT cells. Our results suggest that in ESFT, high CD99 expression levels contribute to the malignant properties of ESFT by promoting growth and migration of tumor cells and identify KCMF1 as a potential metastasis suppressor gene downregulated by high constitutive CD99 expression in ESFT.

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Rapid divergency of rodent CD99 orthologs: Implications for the evolution of the pseudoautosomal region

Cited by 31 publications

References 28 publications

An Essential Role of Sialylated O-Linked Sugar Chains in the Recognition of Mouse CD99 by Paired Ig-Like Type 2 Receptor (PILR)

An Essential Role of Sialylated O-Linked Sugar Chains in the Recognition of Mouse CD99 by Paired Ig-Like Type 2 Receptor (PILR)

Clinical Significance of CD99 Down-Regulation in Gastric Adenocarcinoma

Suppression of KCMF1 by constitutive high CD99 expression is involved in the migratory ability of Ewing's sarcoma cells

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