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Updated: Nov 10, 2025

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence
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Oncogenic mutation or overexpression of oncogenic KRAS or BRAF is not sufficient to confer oncogene addiction

Reina E Ito1,2, Chitose Oneyama3, Kazuhiro Aoki1,2,4

  • 1Quantitative Biology Research Group, Exploratory Research Center on Life and Living Systems (ExCELLS), National Institutes of Natural Sciences, Okazaki, Aichi, Japan.

Plos One
|April 1, 2021
PubMed

Insights

Cancer cells depend on oncogenes for survival, a property called oncogene addiction. This study found that oncogenic mutations or overexpression of KRAS or BRAF alone do not cause oncogene addiction in cells.

Area of Science:

  • Cell Biology
  • Cancer Research
  • Synthetic Biology

Background:

  • Oncogene addiction describes cancer cell dependence on specific oncogenes for survival.
  • Targeting these oncogenes offers a strategy for molecular cancer therapies.
  • The acquisition mechanisms of oncogene addiction remain unclear.

Purpose of the Study:

  • To investigate if oncogenic mutations or oncogene expression are sufficient to induce oncogene addiction.
  • To explore the relationship between transformation activity and oncogene addiction.

Main Methods:

  • Utilized a synthetic biology approach with human mammary MCF-10A cells.
  • Introduced oncogenic KRAS or BRAF mutations (single-allele).
  • Overexpressed oncogenic KRAS and BRAF in MCF-10A cells.

Main Results:

  • Single-allele KRAS/BRAF mutations induced weak transformation but not oncogene addiction.
  • Overexpression of oncogenic KRAS led to transformation but not addiction.
  • Overexpression of oncogenic BRAF did not induce transformation or addiction.

Conclusions:

  • Oncogenic mutation or overexpression of KRAS/BRAF is insufficient for acquiring oncogene addiction.
  • Oncogene addiction is not directly associated with transformation activity.
  • Further research is needed to understand the origins of oncogene addiction.

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