Transforming activity of the RL-akt gene, a c-akt gene activated by long terminal repeat insertion in murine leukemia RL♂1 cells

Motohiko Tanino, Mitsutoshi Matsuo, Akiko Uenaka, Kazunori Tsukuda, Mamoru Oouchida, Eiichi Nakayama, Kenji Shimizu

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4 Citations (Scopus)


The unique antigen peptide pRL1 on BALB/c radiation-induced leukemia RL♂1 cells is derived from the normally untranslated 5' region of the mouse c-akt gene. Insertion of an endogenous long terminal repeat into the first coding exon of the gene resulted in the enhanced production of an altered akt protein, RL-akt, and creation of the tumor rejection antigen peptide pRL1. In this study, we constructed an RL-akt-expressing vector to investigate the transforming ability and anti-apoptotic activity of RK-akt in NIH/3T3 cells. RL-akt-expressing clones formed more colonies than did c-akt-expressing clones in soft agar and exhibited increased saturation density, a lower serum requirement for growth, and tumorigenicity on athymic nude mice. Immunoblot analysis of subcellular protein distribution showed that a considerable proportion of RL-akt was distributed in the membrane fraction. Thus, RL-akt expressed in NIH/3T3 cells appeared to behave like the v-akt oncoprotein. Furthermore, the RL-akt gene conferred resistance to the apoptosis induced by the calcium ionophore A23187 and by ultraviolet irradiation of NIH/3T3 cells. These findings indicate that the RL-akt gene is able to transform cells and exerts an anti-apoptotic effect on recipient cells, thereby implicating the gene in leukemogenesis of RL♂1 cells.

Original languageEnglish
Pages (from-to)286-297
Number of pages12
JournalMolecular Carcinogenesis
Issue number4
Publication statusPublished - 1999



  • Apoptosis
  • Oncogene
  • Serine/threonine protein kinase
  • Tumor antigen

ASJC Scopus subject areas

  • Cancer Research
  • Molecular Biology

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