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LUCA15, a putative tumour suppressor gene encoding an RNA‐binding nuclear protein, is down‐regulated in ras‐transformed Rat‐1 cells
Author(s) -
Edamatsu Hironori,
Kaziro Yoshito,
Itoh Hiroshi
Publication year - 2000
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1046/j.1365-2443.2000.00370.x
Subject(s) - biology , microbiology and biotechnology , gene , ht1080 , carcinogenesis , ectopic expression , gene expression , anti apoptotic ras signalling cascade , somatic cell , regulation of gene expression , oncogene , signal transduction , cell cycle , genetics , mapk/erk pathway
Background The proliferation of mammalian cells is controlled by various intracellular mitogenic signalling pathways. In the intracellular pathways, Ras is involved in the activation of proto‐oncogenes such as an immediate early gene c‐ fos . The somatic mutations of ras genes that elicit the constitutive activation of Ras have been found in tumours. Although these findings suggest that the constitutive activation of Ras‐mediated pathways alters the expression of a set of genes involving tumorigenesis, these genes have not yet fully been studied. Results To study the up‐ or down‐regulated genes in ras ‐transformed cells, we analysed Rat‐1 transfectants expressing Ras(G12V) mutant protein in response to isopropyl‐1‐β‐thio‐ D ‐galactoside using a differential display. We found that the mRNA level of rat homologue of LUCA15 , which has been cloned initially as a putative tumour suppressor gene mapped on human chromosome 3, was down‐regulated by the expression of Ras(G12V). Epitope‐tagged LUCA15 protein was localized in nuclei and had the ability to bind poly(G) RNA homopolymers in vitro . Moreover, ectopic expression of LUCA15 in human fibrosarcoma HT1080 cells suppressed the cell growth. Conclusion These results demonstrate that LUCA15 is one of the down‐regulated genes in ras ‐transformed cells, and suggests that LUCA15 may function as a negative regulator of cell proliferation by the alteration of its mRNA level.