KHU-KIST Department of Converging Science and Technology, Kyung Hee University, Seoul 02447, Korea.
Department of Science in Korean Medicine, Kyung Hee University, 24 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea.
Molecules. 2019 Apr 22;24(8):1584. doi: 10.3390/molecules24081584.
The epithelial-mesenchymal transition (EMT) is a phenomenon that facilitates epithelial cells to acquire invasive potential to induce the initiation the metastatic spread of tumor cells. Here, we determined if brassinin (BSN) can affect the EMT process and deciphered its anti-cancer effects. BSN attenuated the levels of EMT linked genes and suppressed transforming growth factor beta (TGF-β)-mediated regulation of diverse mesenchymal markers. Additionally, BSN did increase the expression of various epithelial marker proteins in lung cancer cells. TGF-β-induced morphological changes and induction of invasive ability of tumor cells was also found to be abrogated by BSN treatment. Finally, BSN not only suppressed constitutive, but also inducible phosphoinositide-3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) phosphorylation in tumor cells.
上皮-间充质转化(EMT)是一种使上皮细胞获得侵袭潜能的现象,从而诱导肿瘤细胞转移扩散的起始。在这里,我们确定了藜芦硫素(BSN)是否可以影响 EMT 过程,并解析了其抗癌作用。BSN 降低了 EMT 相关基因的水平,并抑制了转化生长因子-β(TGF-β)对多种间充质标志物的调节。此外,BSN 确实增加了肺癌细胞中各种上皮标志物蛋白的表达。BSN 处理还发现可以阻止 TGF-β诱导的肿瘤细胞形态变化和侵袭能力的诱导。最后,BSN 不仅抑制了肿瘤细胞中组成性的,而且还抑制了可诱导的磷酸肌醇 3-激酶(PI3K)/蛋白激酶 B(Akt)/雷帕霉素靶蛋白(mTOR)磷酸化。