RBP2 induces epithelial-mesenchymal transition in non-small cell lung cancer

Shikun Wang1, Yang Wang1, Haijian Wu1

  • 1Department of Radiation Oncology, Qilu Hospital of Shandong University, Jinan, Shandong Province, China.

Plos One
|December 31, 2013
PubMed

Insights

Retinoic acid binding protein 2 (RBP2) promotes non-small cell lung cancer progression by inducing epithelial-mesenchymal transition. Targeting RBP2 may offer a new therapeutic strategy for lung cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Retinoic acid binding protein 2 (RBP2) is implicated in various cancers, affecting cell senescence, proliferation, metastasis, and drug tolerance.
  • The specific role of RBP2 in epithelial-mesenchymal transition (EMT) within non-small cell lung cancer (NSCLC) remains unelucidated.

Purpose of the Study:

  • To investigate the impact of RBP2 on epithelial-mesenchymal transition (EMT) in non-small cell lung cancer (NSCLC).
  • To explore the molecular mechanisms by which RBP2 influences EMT markers and signaling pathways in NSCLC.

Main Methods:

  • Analysis of RBP2's effect on E-cadherin and N-cadherin expression in NSCLC cells.
  • Investigation of RBP2's influence on snail expression and Akt signaling pathway activation.
  • Assessment of EMT induction by RBP2 overexpression in NSCLC cell lines.

Main Results:

  • RBP2 was found to down-regulate E-cadherin expression by inhibiting its promoter activity.
  • RBP2 up-regulated N-cadherin and snail expression through activation of the Akt signaling pathway.
  • Overexpression of RBP2 induced epithelial-mesenchymal transition in non-small cell lung cancer cells.

Conclusions:

  • RBP2 plays a significant role in promoting EMT in NSCLC.
  • RBP2's mechanism involves suppressing E-cadherin and activating the Akt/snail pathway, leading to increased N-cadherin.
  • RBP2 represents a potential therapeutic target for developing novel anti-lung cancer treatments.

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