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ckshs expression is linked to cell proliferation in normal and malignant human lymphoid cells
Author(s) -
UrbanowiczKachnowicz Iwona,
Baghdassarian Nathalie,
Nakache Corinne,
Gracia Delphine,
Mekki Yahia,
Bryon Paul André,
Ffrench Martine
Publication year - 1999
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19990702)82:1<98::aid-ijc17>3.0.co;2-a
Subject(s) - cell growth , biology , cyclin dependent kinase 1 , cyclin , cyclin dependent kinase , kinase , cell , microbiology and biotechnology , cell cycle , immunology , cancer research , genetics
Cyclin kinase sub‐units (CKS) are known to interact with cyclin‐dependent kinases (CDKs), but their functions are not completely understood and their expression in human tissues is not documented. For analyzing relationships of CKS with cell proliferation and/or with differentiation, we investigated the expression of ckshs 1 and ckshs 2 in normal and malignant human lymphoid cells. ckshs 1 and ckshs 2 expression appeared to be related to cell proliferation: ( i ) mRNAs increased with stimulation of normal peripheral‐blood lymphocytes, and from the G 1 to the SG 2 M phase in elutriated cells; ( ii ) P9 proteins were also induced by lymphocyte stimulation and were localized in nucleus where phosphorylated forms of CDK1 were also found; ( iii ) in vitro, the phosphorylated forms of CDK1 and CDK2 were preferentially linked to CKS. Among 45 patients presenting acute or chronic lymphoid malignancy, ckshs 1 and ckshs 2 mRNAs varied in a similar way and were significantly correlated to cell proliferation ( p < 0.0001). When analysis was restricted solely to acute lymphoblastic leukemia (ALL) this correlation was still found and ckshs 1 and ckshs 2 were significantly more expressed in T‐cell ALL than in B‐cell‐lineage ALL. These results confirm relationships between ckshs expression and cell proliferation, and pose the question of a link with cell differentiation. Int. J. Cancer 82:98–104, 1999. © 1999 Wiley‐Liss, Inc.