Engagement of CD99 Reduces AP-1 Activity by Inducing BATF in the Human Multiple Myeloma Cell Line RPMI8226.
- Author:
Minchan GIL
1
;
Hyo Kyung PAK
;
Seo Jeong PARK
;
A Neum LEE
;
Young Soo PARK
;
Hyangsin LEE
;
Hyunji LEE
;
Kyung Eun KIM
;
Kyung Jin LEE
;
Dok Hyun YOON
;
Yoo Sam CHUNG
;
Chan Sik PARK
Author Information
- Publication Type:Original Article
- Keywords: CD99; BATF; AP-1; Proliferation; MAP kinase
- MeSH: Breast Neoplasms; Cell Line*; Cyclins; Humans*; Jurkat Cells; Leucine Zippers; Lymphoma; Multiple Myeloma*; Phosphotransferases; Transcription Factor AP-1*; Transcription Factors
- From:Immune Network 2015;15(5):260-267
- CountryRepublic of Korea
- Language:English
- Abstract: CD99 signaling is crucial to a diverse range of biological functions including survival and proliferation. CD99 engagement is reported to augment activator protein-1 (AP-1) activity through mitogen-activated protein (MAP) kinase pathways in a T-lymphoblastic lymphoma cell line Jurkat and in breast cancer cell lines. In this study, we report that CD99 differentially regulated AP-1 activity in the human myeloma cell line RPMI8226. CD99 was highly expressed and the CD99 engagement led to activation of the MAP kinases, but suppressed AP-1 activity by inducing the expression of basic leucine zipper transcription factor, ATF-like (BATF), a negative regulator of AP-1 in RPMI8226 cells. By contrast, engagement of CD99 enhanced AP-1 activity and did not change the BATF expression in Jurkat cells. CD99 engagement reduced the proliferation of RPMI8226 cells and expression of cyclin 1 and 3. Overall, these results suggest novel CD99 functions in RPMI8226 cells.
