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Decreased RIZ1 expression but not RIZ2 in hepatoma and suppression of hepatoma tumorigenicity by RIZ1
Author(s) -
Jiang Guangliang,
Liu Limin,
Buyse Inge M.,
Simon Daniela,
Huang Shi
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(19991112)83:4<541::aid-ijc17>3.0.co;2-f
Subject(s) - cancer research , tumor suppressor gene , biology , suppressor , gene , gene product , cancer , cell culture , apoptosis , cell growth , microbiology and biotechnology , gene expression , genetics , carcinogenesis
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 G 2 /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 G 2 /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.