Forced Expression of YL-1 Protein Suppresses the Anchorage-Independent Growth of Kirsten Sarcoma Virus-Transformed NIH3T3 Cells

Izumi Horikawa, Hiromi Tanaka, Yoshihiro Yuasa, Mikio Suzuki, Motoyuki Shimizu, Mitsuo Oshimura

Research output: Contribution to journalArticle

9 Scopus citations

Abstract

The YL-1 gene, encoding a novel nuclear protein with transcription factor-like features, has been isolated from the human chromosome 1q21, one of the regions supposedly carrying a transformation suppressor gene(s) for Kirsten sarcoma virus-transformed NIH3T3 (DT) cells. To test the suppressive activity of the YL-1 gene product, we forced the expression of human YL-1 cDNA in DT cells. The anchorage-independent growth (colony-forming ability in soft agar medium) was markedly suppressed in cells highly expressing the exogenous human YL-1 protein. Moreover, the soft agar clones, which were rarely originated from these cells, expressed reduced levels of exogenous YL-1 or none, with or without the loss/rearrangement of the introduced cDNA. In control experiments, cells carrying an introduced vector alone or an antisense-strand expression plasmid grew in soft agar as efficiently as parental DT cells. In contrast to the suppression of anchorage-independent growth, the forced expression of YL-1 did not affect the transformed phenotypes in adherent culture and tumorigenicity in nude mice. These findings not only indicated that the YL-1 protein functions as a transformation suppressor, but also suggest that it may be important for elucidating anchorage independence under separate genetic control from other transformed phenotypes.

Original languageEnglish (US)
Pages (from-to)11-17
Number of pages7
JournalExperimental Cell Research
Volume220
Issue number1
DOIs
StatePublished - Sep 1995

ASJC Scopus subject areas

  • Cell Biology

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