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Identification of CM1 as a Pathogenic Factor in Inflammatory Diseases and Cancer : Identification of CM1 as a Pathogenic Factor in Inflammatory Diseases and Cancer

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Authors

Bae, Seyeon; Kim, Hyemin; Yu, Yeon Sil; Lee, Na-Eun; Kong, Koo Myoung; Kim, Hang-Rae; Hwang, Young-Il; Song, Yeong Wook; Kang, Jae Seung; Lee, Wang Jae

Issue Date
2011-06
Publisher
대한면역학회
Citation
Immune Network, Vol.11 No.3, pp.175-181
Abstract
Background: CM1 (centrocyte/-blast marker 1) was defined by a mAb against concavabalin-A (ConA) activated PBMC. It is expressed in germinal center of human tonsil and on the surface of activated PBMC as well as cancer cells. Recently,increased productions of pro-inflammatory mediators were detected from activated PBMC by CM1 ligation. Methods:However, there is a limitation to explain the exact role of CM1 on inflammation and its related mechanisms, since the identity of CM1 is still not clarified. In our previous study, we have already confirmed that soluble form of CM1 was produced by Raji. Therefore, we performed Q-TOF analysis after immunoprecipitation of concentrated Raji culture supernatant using anti-CM1 mAbs. Results: As a result, we found that CM1 is identical to enolase-1(ENO1), a glycolytic enzyme,and we confirmed that results by silencing ENO1 using siRNA. It was also confirmed through competition assay between anti-CM1 and anti-ENO1 mAbs. Finally, we investigated the possible role of CM1 in inflammatory response and cancer. The ligation of CM1 on Raji cells with anti-CM1mAbs induces the extensive production of prostaglandin E2(PGE2). In addition, the increased activity of matrix metalloproteinase (MMP)-2/9 was shown in NCI-N87, stomach cancer cell line by CM1 stimulation. Conlusion: CM1 is identical to ENO1 and it might be an important role in the regulation of inflammatory responses.
ISSN
1598-2629
URI
https://hdl.handle.net/10371/202679
DOI
https://doi.org/10.4110/in.2011.11.3.175
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Research Area Function, Immune modulation by metabolites, T-cell anergy, differentiation of memory CD8+ T cells, metabolism

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