Hematopoietic malignancies associated with increased Stat5 and Bcl-x L expressions in Ink4a/Arf-deficient mice

Hoon Sung Young, Junghwan Park, Bongkun Choi, Jaehong Kim, Cheolho Cheong, Sik Choi Yoon, Young Yang Eun, Minjae Lee, Soo Han Jin, Chul Park Sang, Tae Hee Han, Jin Kim Tae, Jaewhan Song, Kunsoo Rhee, Han Woong Lee

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)

Abstract

The INK4a/ARF locus, which encodes the two distinct proteins p16 INK4a and p14ARF, is frequently altered in various hematological malignancies as well as in other types of cancers in humans. In this study, we surveyed tumors that had spontaneously developed in Ink4a/Arf-deficient mice with an inbred FVB/NJ genetic background. We found that an Ink4a/Arf-deficiency exerted more severe effects on the induction of hematopoietic malignancies in mice with an inbred FVB/NJ genetic background than in mice with a mixed genetic background. We also provided the evidence that this prevalence of hematopoietic malignancies in Ink4a/Arf-deficient mice is associated with the upregulated expressions of Stat5 and its transcriptional target, Bcl-xL, both of which are involved in the regulation of hematopoiesis. These results suggest a possible implication of the Ink4a/Arf locus in the control of hematopoietic pathways by negatively regulating the Stat5-signalling pathways.

Original languageEnglish
Pages (from-to)732-739
Number of pages8
JournalMechanisms of Ageing and Development
Volume126
Issue number6-7
DOIs
Publication statusPublished - 2005 Jun

Bibliographical note

Funding Information:
This work was supported by the grants from the Ministry of Health and Welfare (02-PJ1-PG3-21001-0007), 21C Frontier Functional Human Genome Project (FG01-0304-002-1-0-0) and BRC-frontier (M103KV010018-03K2201-01830) from the Ministry of Science and Technology, Korea Science and Engineering Foundation through the Science Research Center–Molecular Therapy Research Center, and Korea Research Foundation (015-C00398).

All Science Journal Classification (ASJC) codes

  • Ageing
  • Developmental Biology

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