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Tumor Milieu Controlled by RB Tumor Suppressor

Shunsuke Kitajima1,2, Fengkai Li3, Chiaki Takahashi3

  • 1Department of Cell Biology, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo 135-8550, Japan.

International Journal of Molecular Sciences
|April 5, 2020
PubMed

Insights

The RB protein, beyond cell cycle control, influences cancer aggressiveness. RB inactivation promotes inflammation and shapes the tumor microenvironment, impacting cancer progression and immunotherapy potential.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • The RB gene is frequently mutated in human cancers, traditionally linked to cell cycle regulation.
  • RB gene aberrations often correlate with aggressive cancer phenotypes like metastasis and drug resistance, suggesting cell cycle-independent roles.
  • RB protein's functions extend beyond cell cycle control, influencing tumor lineage plasticity, metabolism, and the tumor microenvironment (TME).

Purpose of the Study:

  • To review the multifaceted functions of the RB protein.
  • To focus on RB's role in controlling the tumor microenvironment (TME).
  • To discuss the non-cell-autonomous functions of RB and their clinical relevance to cancer immunotherapy.

Main Methods:

  • Literature review focusing on RB gene functions in cancer.
  • Analysis of RB's role in tumor lineage plasticity, metabolism, and TME.
  • Examination of RB's impact on cytokine production and reactive oxygen species (ROS).

Main Results:

  • RB inactivation enhances pro-inflammatory cytokine production (e.g., CCL2) via mitochondrial ROS.
  • RB inactivation promotes both cell-autonomous cancer growth and non-cell-autonomous TME reprogramming.
  • RB's non-cell-autonomous functions contribute to a pro-tumorigenic niche.

Conclusions:

  • RB plays a critical role in regulating the TME through non-cell-autonomous mechanisms.
  • RB inactivation drives cancer aggressiveness by modulating inflammation and the TME.
  • Understanding RB's non-cell-autonomous functions may offer new avenues for cancer immunotherapy.
Keywords:
CCL2reactive oxygen speciesretinoblastomatumor microenvironment

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