Wang Shikun, Wang Yang, Wu Haijian, Hu Likuan
Department of Radiation Oncology, Qilu Hospital of Shandong University, Jinan, Shandong Province, China.
PLoS One. 2013 Dec 20;8(12):e84735. doi: 10.1371/journal.pone.0084735. eCollection 2013.
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.
研究发现,视黄醇结合蛋白2(RBP2)积极参与癌症进展。它能抑制癌细胞衰老,介导癌细胞增殖并促进癌症转移。它对药物耐受性也至关重要。然而,RBP2对上皮-间质转化的影响仍不清楚。在本研究中,我们分析了RBP2对非小细胞肺癌上皮-间质转化的影响。结果表明,RBP2通过抑制E-钙黏蛋白的启动子活性下调其表达,并通过激活Akt信号上调N-钙黏蛋白和蜗牛蛋白的表达,RBP2的过表达诱导非小细胞肺癌细胞发生上皮-间质转化。我们的研究进一步表明,RBP2可能是抗肺癌治疗的潜在靶点。