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Updated: May 4, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
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.
Abstract:
RBP2 has been found to actively participate in cancer progression. It inhibits the senescence of cancer cells, mediates cancer cell proliferation and promotes cancer metastasis. It is also essential to drug tolerance. However, the effects of RBP2 on epithelial-mesenchymal transition are still unknown. In this study, we analyzed the effects of RBP2 on epithelial-mesenchymal transition in non-small cell lung cancer. The results showed that RBP2 down-regulated the expression of E-cadherin by inhibiting the promoter activity of E-cadherin and up-regulated the expression of N-cadherin and snail via the activation of Akt signaling, and the overexpression of RBP2 induced epithelial-mesenchymal transition in non-small cell lung cancer cells. Our study further indicated that RBP2 may be a potential target for anti-lung cancer therapy.
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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