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H3K9 methyltransferases and demethylases control lung tumor-propagating cells and lung cancer progression

S P Rowbotham1,2, F Li3, A F M Dost1,2

  • 1Stem Cell Program, Division of Hematology/Oncology and Pulmonary and Respiratory Diseases, Children's Hospital Boston, Boston, MA, 02115, USA.

Nature Communications
|November 21, 2018
PubMed

Insights

Inhibiting histone methyltransferase G9a promotes aggressive lung cancer by increasing tumor-propagating cells. Targeting histone demethylases, not G9a, offers a safer and more effective strategy for lung adenocarcinoma treatment.

Area of Science:

  • Oncology
  • Epigenetics
  • Cancer Biology

Background:

  • Epigenetic regulators are promising anticancer targets, but their therapeutic efficacy in vivo and consideration of tumor heterogeneity remain unproven.
  • Histone methyltransferase G9a is a proposed therapeutic target in various cancers.

Purpose of the Study:

  • To investigate the role of G9a in lung adenocarcinoma.
  • To evaluate the therapeutic potential of targeting G9a and histone demethylases in lung cancer.

Main Methods:

  • Studied the effects of G9a inhibition and depletion on lung adenocarcinoma cells and tumor progression in vivo.
  • Investigated the impact of histone demethylase depletion on G9a-regulated genes and TPC phenotypes.

Main Results:

  • G9a inhibition drives lung adenocarcinoma cells towards a tumor-propagating cell (TPC) phenotype by upregulating extracellular matrix genes.
  • G9a depletion enriches tumors with TPCs, accelerating lung cancer progression and metastasis.
  • Depleting histone demethylases represses G9a-regulated genes and TPC phenotypes, impairing tumor progression.

Conclusions:

  • G9a inhibition is detrimental in certain lung cancer contexts, promoting aggressive tumor-propagating cells.
  • Targeting histone demethylases presents a more promising therapeutic strategy for lung adenocarcinoma.
  • Understanding tumor cell context is crucial for developing effective epigenetic therapies in cancer.

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