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Cellular and Molecular Biology 69: Inhibitors of Signal Transduction in Cancer

Abstract #5082

Opposite effect of the external Qi of Yan Xin Qigong on the Akt and ERK pathways in cancer versus normal cells: Differential cytotoxic effect.

Institute of Chongqing Traditional Chinese Medicine, Chongqing, China, New Medical Science Research Institute, New York, NY, Massachusetts General Hospital and Harvard Medical School, Boston, MA, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, Children’s Hospital Boston and Harvard Medical School, Boston, MA

Long-term clinical observations and progress from ongoing studies have shown that the cancer patients received significant benefit from the exposure to the external Qi of Yan Xin Qigong (YXQ) originated from traditional Chinese medicine. In some typical cases, patients with clinically diagnosed aggressive and recurrent tumors have been surviving for >10-20 years after the treatment by the external Qi of YXQ. Furthermore, the external Qi of YXQ helps patients improve or avoid side effects associated with conventional radio- and chemotherapy. However, the molecular mechanisms underlying these beneficial effects largely remain to be explored. We have investigated the cytotoxic effect of the external Qi of YXQ on MDA-MB-231 breast cancer cells, BxPC3 pancreatic cancer cells and A172 glioma cells, and the effect of YXQ external Qi on the Akt and extracellular signal-regulated kinase (ERK) pathways that have been shown to play an important role in cancer cell survival, proliferation, and chemoresistance. Cell viability assays showed that the external Qi of YXQ had potent cytotoxicity towards all these cancer cells, but had no cytotoxic effect on fibroblasts and human umbilical vein endothelial cells (HUVEC). The external Qi of YXQ dramatically reduced phosphorylation of Akt and ERK1/2 kinases in these cancer cells under normal growth conditions, and inhibits epidermal growth factor (EGF)-mediated phosphorylation of ERK1/2 kinases. It also suppressed the basal and inducible NF-B activity in BxPC3 cells, and attenuated expression of NF-B target genes including antiapoptotic Bcl-2, Bcl-xL and XIAP. In contrast, the external Qi of YXQ transiently stimulated phosphorylation of Akt and ERK1/2 kinases in serum-starved fibroblasts and HUVEC. It also increased expression of heat shock protein 70 in these normal cells. These findings demonstrate that the external Qi of YXQ has opposite effects on the Akt and ERK pathways in cancer versus normal cells. Inhibition of these pathways may at least partly be responsible for the cytotoxic effect of the external Qi of YXQ on cancer cells, while activation of these pathways could be protective for normal cells. The external Qi of YXQ could thus potentially be an effective approach for targeted therapy of breast, brain and pancreatic cancer.