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Rnd3 regulates lung cancer cell proliferation through notch signaling

Yongjun Tang1, Chengping Hu1, Huaping Yang1

  • 1Department of Respiratory Medicine, Xiangya Hospital, the Central South University, Changsha, Hunan, P.R. China.

Plos One
|November 6, 2014
PubMed

Insights

Rnd3 protein is down-regulated in non-small cell lung cancer (NSCLC), promoting cell proliferation via Notch signaling. Restoring Rnd3 or inhibiting Notch blocks cancer growth.

Area of Science:

  • Cell Biology
  • Molecular Oncology

Background:

  • Rnd3/RhoE is a Rho GTPase regulating cell functions.
  • Rnd3 dysregulation is linked to cancer development and metastasis.
  • Non-small cell lung cancer (NSCLC) is a leading cause of cancer mortality worldwide.

Purpose of the Study:

  • To investigate the expression and role of Rnd3 in NSCLC.
  • To explore the molecular mechanisms underlying Rnd3's function in NSCLC.

Main Methods:

  • Analysis of Rnd3 expression in NSCLC cell lines (H358, H520, A549).
  • Assessment of Rho Kinase and Notch signaling pathway activation.
  • Evaluation of cell proliferation following Rnd3 reintroduction or pathway inhibition.
  • Investigation of Rnd3's effect on Notch intracellular domain (NICD) protein levels.

Main Results:

  • Rnd3 expression was significantly down-regulated in tested NSCLC cell lines.
  • Rnd3 down-regulation correlated with hyper-activation of Rho Kinase and Notch signaling.
  • Rnd3 reintroduction or Notch inhibition, but not Rho Kinase inhibition, suppressed NSCLC cell proliferation.
  • Rnd3 was found to mediate proteasomal degradation of NICD, thereby regulating its abundance.

Conclusions:

  • Rnd3 functions as a tumor suppressor in NSCLC.
  • Rnd3 inhibits NSCLC cell proliferation primarily through the Notch1/NICD/Hes1 pathway, independent of Rho Kinase.
  • Targeting the Rnd3-Notch axis presents a potential therapeutic strategy for NSCLC.

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