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Matrix Stiffness Regulates TGFβ1-Induced αSMA Expression via a G9a-LATS-YAP Signaling Cascade.

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Matrix stiffness and TGF-β1 signaling regulate the G9a methyltransferase, impacting cancer and fibrosis progression. This study reveals a G9a-LATS-YAP cascade controlling cell responses to matrix mechanics.

Keywords:
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Area of Science:

  • Biochemistry
  • Cell Biology
  • Cancer Research

Background:

  • Extracellular matrix (ECM) stiffness is altered in cancer and fibrosis.
  • The role of matrix mechanics in regulating the G9a methyltransferase and its downstream signaling remains poorly understood.

Purpose of the Study:

  • To investigate how matrix stiffness and transforming growth factor (TGF)-β1 signaling influence G9a expression and activity.
  • To elucidate the signaling pathways involved in the cellular response to ECM mechanics.

Main Methods:

  • Culturing mammary epithelial cells on substrata of varying stiffness.
  • Modulating G9a expression and activity.
  • Assessing levels of histone mark H3K9me2.
  • Analyzing expression of alpha smooth muscle actin (αSMA), N-cadherin, large tumor suppressor kinase 2 (LATS2), and the nuclear localization of yes associated protein (YAP).

Main Results:

  • Matrix stiffness and TGF-β1 signaling synergistically regulate G9a expression and H3K9me2 levels.
  • G9a suppression attenuates TGF-β1-induced αSMA, N-cadherin expression, and morphological changes in mammary epithelial cells on stiff matrices.
  • G9a knockdown increases LATS2 expression and reduces YAP nuclear localization.
  • LATS inhibition enhances YAP nuclear localization and αSMA expression, while YAP inhibition reduces αSMA expression.

Conclusions:

  • A signaling cascade involving G9a, LATS, and YAP mediates mammary epithelial cell responses to ECM stiffness and TGF-β1.
  • This pathway plays a critical role in regulating cellular behavior in the context of altered matrix mechanics relevant to fibrosis and cancer.