Journal article
Decreased RIZ1 expression but not RIZ2 in hepatoma and suppression of hepatoma tumorigenicity by RIZ1
International journal of cancer, v 83(4), pp 541-546
12 Nov 1999
PMID: 10508492
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
The distal short arm of human chromosome 1 (1p36) is commonly altered in primary hepatoma tumors and cell lines. This region includes the RIZ gene, a member of the PR (PRDI‐BF1/BLIMP1 and RIZ homology) domain family of transcription factors. An unusual feature of this family is the yin‐yang involvement in human cancers. Two products are normally produced from a PR family member which differ by the presence or absence of the PR domain; the PR‐plus product is disrupted or underexpressed whereas the PR‐minus product is present or overexpressed in cancer cells. The PR‐plus product RIZ1 is a candidate tumor suppressor because it can induce G2/M arrest and/or apoptosis and is commonly underexpressed in breast cancer. Here, we have investigated the role of RIZ in hepatoma. RIZ1 transcript was undetectable in 80% of hepatoma cell lines (8 of 10 lines examined). RIZ1 expression was also decreased in hepatoma tumor specimens. In contrast, RIZ2 transcript was uniformly present in all samples examined. Adenovirus‐mediated RIZ1 expression in hepatoma cell lines caused cell cycle arrest in G2/M and/or programmed cell death. RIZ1 expression also suppressed tumorigenicity of hepatoma cells in nude mice. Our observations reinforce the yin‐yang notion of RIZ gene products in human cancer and suggest a RIZ1 tumor suppressor role in hepatoma. Int. J. Cancer 83:541–546, 1999. © 1999 Wiley‐Liss, Inc.
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Details
- Title
- Decreased RIZ1 expression but not RIZ2 in hepatoma and suppression of hepatoma tumorigenicity by RIZ1
- Creators
- Guang‐liang JiangLimin Liu - Sanford Burnham Prebys Medical Discovery InstituteInge M. Buyse - Sanford Burnham Prebys Medical Discovery InstituteDaniela Simon - Hahnemann University HospitalShi Huang - Sanford Burnham Prebys Medical Discovery InstituteDonald R Simon - Communication
- Publication Details
- International journal of cancer, v 83(4), pp 541-546
- Publisher
- John Wiley & Sons, Inc
- Number of pages
- 6
- Grant note
- Tobacco‐Related Disease Research Program of the University of California (7RT‐0026) NIH (RO1‐CA57496; RO1‐CA76146)
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Communication
- Web of Science ID
- WOS:000083220000017
- Other Identifier
- 991019168264704721
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- Collaboration types
- Domestic collaboration
- Web of Science research areas
- Oncology