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

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

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
Volume26
Issue number4
Publication statusPublished - 1999

Fingerprint

Terminal Repeat Sequences
Leukemia
NIH 3T3 Cells
Genes
Nude Mice
Radiation-Induced Leukemia
Clone Cells
Peptides
Calcium Ionophores
5' Untranslated Regions
Oncogene Proteins
Calcimycin
Neoplasm Antigens
Agar
Exons
Proteins
Apoptosis
Antigens
Membranes
Growth

Keywords

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

ASJC Scopus subject areas

  • Cancer Research
  • Molecular Biology

Cite this

Transforming activity of the RL-akt gene, a c-akt gene activated by long terminal repeat insertion in murine leukemia RL♂1 cells. / Tanino, Motohiko; Matsuo, Mitsutoshi; Uenaka, Akiko; Tsukuda, Kazunori; Oouchida, Mamoru; Nakayama, Eiichi; Shimizu, Kenji.

In: Molecular Carcinogenesis, Vol. 26, No. 4, 1999, p. 286-297.

Research output: Contribution to journalArticle

Tanino, Motohiko ; Matsuo, Mitsutoshi ; Uenaka, Akiko ; Tsukuda, Kazunori ; Oouchida, Mamoru ; Nakayama, Eiichi ; Shimizu, Kenji. / Transforming activity of the RL-akt gene, a c-akt gene activated by long terminal repeat insertion in murine leukemia RL♂1 cells. In: Molecular Carcinogenesis. 1999 ; Vol. 26, No. 4. pp. 286-297.
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