ST2 gene products critically contribute to cellular transformation caused by an oncogenic Ras mutant

Kenji Tago, Satoshi Ohta, Masaki Kashiwada, Megumi Tago, Jitsuhiro Matsugi, Shin ichi Tominaga, Ken Yanagisawa

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

The ST2 gene was originally identified as a primary responsive gene, and the expressions of its gene products are induced by stimulation with growth factors and by oncogenic stresses. In this study, we observed that oncogenic Ras mutant induced the expression of ST2 and ST2L proteins. Interestingly, the enforced expression of ST2 gene products in NIH-3T3 murine fibroblasts remarkably enhanced Ras (G12 V)-induced cellular transformation. Furthermore, when the expression of ST2 gene products was silenced by RNA-interference technique, Ras (G12 V)-induced cellular transformation was drastically suppressed. According to these observations, it was indicated that the oncogenic Ras-induced expression of ST2 gene products is required for the acceleration of cellular transformation, and this seems to be independent of the stimulation with IL-33, a ligand for ST2/ST2L. Interestingly, knockdown of ST2 gene products caused a reduction in Rb phosphorylation in transformed murine fibroblasts, suggesting the functional involvement of ST2 gene products in cell cycle progression during cellular transformation. Our current study strongly suggests the importance of ST2 gene products in cellular transformation, and the presence of novel mechanism how ST2 gene products affect the cellular transformation and cell proliferation.

Original languageEnglish
JournalHeliyon
DOIs
Publication statusAccepted/In press - 2017

Fingerprint

Gene Expression
Genes
Fibroblasts
Cell Proliferation
Gene Knockdown Techniques
RNA Interference
Intercellular Signaling Peptides and Proteins
Cell Cycle
Phosphorylation
Ligands
Proteins
Interleukin-33

Keywords

  • Cancer research
  • Cell biology

ASJC Scopus subject areas

  • General

Cite this

ST2 gene products critically contribute to cellular transformation caused by an oncogenic Ras mutant. / Tago, Kenji; Ohta, Satoshi; Kashiwada, Masaki; Tago, Megumi; Matsugi, Jitsuhiro; Tominaga, Shin ichi; Yanagisawa, Ken.

In: Heliyon, 2017.

Research output: Contribution to journalArticle

Tago, Kenji ; Ohta, Satoshi ; Kashiwada, Masaki ; Tago, Megumi ; Matsugi, Jitsuhiro ; Tominaga, Shin ichi ; Yanagisawa, Ken. / ST2 gene products critically contribute to cellular transformation caused by an oncogenic Ras mutant. In: Heliyon. 2017.
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AU - Ohta, Satoshi

AU - Kashiwada, Masaki

AU - Tago, Megumi

AU - Matsugi, Jitsuhiro

AU - Tominaga, Shin ichi

AU - Yanagisawa, Ken

PY - 2017

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AB - The ST2 gene was originally identified as a primary responsive gene, and the expressions of its gene products are induced by stimulation with growth factors and by oncogenic stresses. In this study, we observed that oncogenic Ras mutant induced the expression of ST2 and ST2L proteins. Interestingly, the enforced expression of ST2 gene products in NIH-3T3 murine fibroblasts remarkably enhanced Ras (G12 V)-induced cellular transformation. Furthermore, when the expression of ST2 gene products was silenced by RNA-interference technique, Ras (G12 V)-induced cellular transformation was drastically suppressed. According to these observations, it was indicated that the oncogenic Ras-induced expression of ST2 gene products is required for the acceleration of cellular transformation, and this seems to be independent of the stimulation with IL-33, a ligand for ST2/ST2L. Interestingly, knockdown of ST2 gene products caused a reduction in Rb phosphorylation in transformed murine fibroblasts, suggesting the functional involvement of ST2 gene products in cell cycle progression during cellular transformation. Our current study strongly suggests the importance of ST2 gene products in cellular transformation, and the presence of novel mechanism how ST2 gene products affect the cellular transformation and cell proliferation.

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