Yan Xin, Shen Hua, Jiang Hongjian, Hu Dan, Zhang Chengsheng, Wang Jun, Wu Xinqi
Chongqing Institute of Traditional Chinese Medicine, Chongqing.
Cell Physiol Biochem. 2010;25(2-3):263-70. doi: 10.1159/000276560. Epub 2010 Jan 12.
The antitumor effects of external Qi of Yan Xin Qigong (YXQ-EQ) have been widely described over the past three decades. To gain a better understanding of the mechanisms underlying YXQ-EQ's antitumor effects, in the present study we investigated its effects on growth, migration, invasion and apoptosis of breast cancer cells and the underlying molecular mechanisms. We show that YXQ-EQ treatment caused a time-dependent reduction in viability, blocked clonogenic growth and induced apoptosis in estrogen-independent breast cancer MDA-MB-231 cells. Furthermore, YXQ-EQ treatment blocked migration and invasion of MDA-MB-231 cells. Biochemically, YXQ-EQ treatment markedly inhibited constitutive and EGF-induced Akt phosphorylation. YXQ-EQ also substantially repressed NF-kappaB activity, resulting in decreased expression of anti-apoptotic Bcl-2, Bcl-X(L), XIAP and survivin proteins. These findings suggest that YXQ-EQ may induce apoptosis and inhibition of migration and invasion of MDA-MB-231 cells through the repression of Akt/NF-kappaB signaling.
在过去三十年里,严新气功外气(YXQ-EQ)的抗肿瘤作用已被广泛报道。为了更好地理解YXQ-EQ抗肿瘤作用的潜在机制,在本研究中,我们调查了其对乳腺癌细胞生长、迁移、侵袭和凋亡的影响以及潜在的分子机制。我们发现,YXQ-EQ处理导致雌激素非依赖性乳腺癌MDA-MB-231细胞的活力随时间下降,抑制克隆生长并诱导凋亡。此外,YXQ-EQ处理阻止了MDA-MB-231细胞的迁移和侵袭。生化分析表明,YXQ-EQ处理显著抑制组成型和表皮生长因子(EGF)诱导的Akt磷酸化。YXQ-EQ还显著抑制核因子κB(NF-κB)活性,导致抗凋亡蛋白Bcl-2、Bcl-X(L)、X连锁凋亡抑制蛋白(XIAP)和生存素表达降低。这些发现表明,YXQ-EQ可能通过抑制Akt/NF-κB信号传导诱导MDA-MB-231细胞凋亡并抑制其迁移和侵袭。