title: Engagement of CD99 Reduces AP-1 Activity by Inducing BATF in the Human Multiple Myeloma Cell Line RPMI8226.
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.
authors.affiliation: Cell Dysfunction Research Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
authors.forename: Minchan
authors.initials: M
authors.lastname: Gil
authors.affiliation: Cell Dysfunction Research Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
authors.forename: Hyo-Kyung
authors.initials: HK
authors.lastname: Pak
authors.affiliation: Cell Dysfunction Research Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
authors.forename: Seo-Jeong
authors.initials: SJ
authors.lastname: Park
authors.affiliation: Cell Dysfunction Research Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
authors.forename: A-Neum
authors.initials: AN
authors.lastname: Lee
authors.affiliation: Department of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
authors.forename: Young-Soo
authors.initials: YS
authors.lastname: Park
authors.affiliation: Cell Dysfunction Research Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
authors.forename: Hyangsin
authors.initials: H
authors.lastname: Lee
authors.affiliation: Cell Dysfunction Research Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
authors.forename: Hyunji
authors.initials: H
authors.lastname: Lee
authors.affiliation: SIS Immunology Research Center, Sookmyung Women's University, Seoul 04310, Korea.
authors.forename: Kyung-Eun
authors.initials: KE
authors.lastname: Kim
authors.affiliation: Institute for Life Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
authors.forename: Kyung Jin
authors.initials: KJ
authors.lastname: Lee
authors.affiliation: Department of Oncology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
authors.forename: Dok Hyun
authors.initials: DH
authors.lastname: Yoon
authors.affiliation: Department of Otolaryngology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
authors.forename: Yoo-Sam
authors.initials: YS
authors.lastname: Chung
authors.affiliation: Cell Dysfunction Research Center, University of Ulsan College of Medicine, Seoul 05505, Korea. ; Department of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
authors.forename: Chan-Sik
authors.initials: CS
authors.lastname: Park
keywords: AP-1; BATF; CD99; MAP kinase; Proliferation