Soluble SLAMF7 promotes the growth of myeloma cells via homophilic interaction with surface SLAMF7.


Journal

Leukemia
ISSN: 1476-5551
Titre abrégé: Leukemia
Pays: England
ID NLM: 8704895

Informations de publication

Date de publication:
01 2020
Historique:
received: 14 11 2018
accepted: 04 06 2019
revised: 24 04 2019
pubmed: 31 7 2019
medline: 2 7 2020
entrez: 31 7 2019
Statut: ppublish

Résumé

SLAMF7 is expressed mainly on multiple myeloma (MM) cells and considered an ideal target for immunotherapeutic approaches. Indeed, elotuzumab, an anti-SLAMF7 antibody, is used for the treatment of MM in combination with immunomodulatory drugs. SLAMF7 is cleaved via unknown mechanisms and detected as a soluble form (sSLAMF7) exclusively in the serum of MM patients; however, little is known about the role of sSLAMF7 in MM biology. In this study, we found that sSLAMF7 enhanced the growth of MM cells via homophilic interaction with surface SLAMF7 and subsequent activation of the SHP-2 and ERK signaling pathways. Elotuzumab suppressed sSLAMF7-induced MM cell growth both in vitro and in vivo. Promoter analyses identified IKZF1 (Ikaros) as a pivotal transcriptional activator of the SLAMF7 gene. Pharmacological targeting of Ikaros by lenalidomide and its analog pomalidomide downregulated SLAMF7 expression and ameliorated the response of MM cells to sSLAMF7. Elotuzumab blocked the growth-promoting function of sSLAMF7 when combined with lenalidomide in a murine xenograft model. Neutralization of sSLAMF7 is a novel antimyeloma mechanism of elotuzumab, which is enhanced by immunomodulatory drugs via downregulation of surface SLAMF7 expression on MM cells. These findings may provide important information for the optimal use of elotuzumab in MM treatment.

Identifiants

pubmed: 31358854
doi: 10.1038/s41375-019-0525-6
pii: 10.1038/s41375-019-0525-6
doi:

Substances chimiques

Antibodies, Monoclonal, Humanized 0
SLAMF7 protein, human 0
Signaling Lymphocytic Activation Molecule Family 0
elotuzumab 1351PE5UGS
Thalidomide 4Z8R6ORS6L
pomalidomide D2UX06XLB5
Lenalidomide F0P408N6V4

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

180-195

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Auteurs

Jiro Kikuchi (J)

Division of Stem Cell Regulation, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Tochigi, 329-0498, Japan.

Mitsuo Hori (M)

Department of Hematology, Ibaraki Prefectural Central Hospital, Kasama, Ibaraki, 309-1793, Japan.

Hidekatsu Iha (H)

Department of Microbiology, Oita University Faculty of Medicine, Yufu, Oita, 879-5593, Japan.

Noriko Toyama-Sorimachi (N)

Department of Molecular Immunology and Inflammation, Research Institute, National Center for Global Health and Medicine, Shinjuku, Tokyo, 162-8655, Japan.

Shotaro Hagiwara (S)

Department of Hematology, Tokyo Women's Medical University, Shinjuku, Tokyo, 162-8666, Japan.

Yoshiaki Kuroda (Y)

Division of Stem Cell Regulation, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Tochigi, 329-0498, Japan.

Daisuke Koyama (D)

Division of Stem Cell Regulation, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Tochigi, 329-0498, Japan.

Tohru Izumi (T)

Division of Hematology, Tochigi Cancer Center, Utsunomiya, Tochigi, 320-0834, Japan.

Hiroshi Yasui (H)

The Institute of Medical Science, The University of Tokyo, Minato, Tokyo, 108-8639, Japan.

Atsushi Suzuki (A)

Oncology Division, Bristol-Myers Squibb K.K., Shinjuku, Tokyo, 163-1327, Japan.

Yusuke Furukawa (Y)

Division of Stem Cell Regulation, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Tochigi, 329-0498, Japan. furuyu@jichi.ac.jp.

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