美國(guó)研究人員4月15日說(shuō),，傳統(tǒng)中國(guó)醫(yī)學(xué)已使用數(shù)百年的針裂蹄木層孔菌可能具有阻止乳腺癌細(xì)胞生長(zhǎng)的功效,，有望成為抗擊乳腺癌的新“武器”。
美國(guó)研究人員所做的細(xì)胞實(shí)驗(yàn)顯示,，針裂蹄木層孔菌具有抗乳腺癌細(xì)胞的功效,。研究人員認(rèn)為，這種藥材可能通過(guò)抑制“AKT”酶抗擊乳腺癌細(xì)胞,，“AKT”酶可控制促使細(xì)胞生長(zhǎng)的“信號(hào)”,。
路透社報(bào)道說(shuō)，科學(xué)界此前已發(fā)現(xiàn)針裂蹄木層孔菌有抗皮膚癌,、肺癌和前列腺癌的功效,，但這項(xiàng)針對(duì)乳腺癌的新研究標(biāo)志研究人員開(kāi)始了解針裂蹄木層孔菌的抗癌機(jī)理。
美國(guó)印第安納波利斯地區(qū)一個(gè)研究所的科研人員丹尼爾·斯利瓦說(shuō),，實(shí)驗(yàn)中,，針裂蹄木層孔菌提取物減慢了新生癌細(xì)胞的生長(zhǎng)速度，阻止了向腫瘤提供養(yǎng)分的新生血管的產(chǎn)生,。
斯利瓦說(shuō)：“我們還沒(méi)有能力把這些知識(shí)應(yīng)用于當(dāng)代醫(yī)學(xué)……希望我們的研究將鼓勵(lì)更多研究者探索如何把可入藥的菌類(lèi)應(yīng)用于治療癌癥,。”斯利瓦等人的研究成果刊登在《英國(guó)癌癥雜志》（British Journal of Cancer）上。（來(lái)源：新華網(wǎng)）
生物谷推薦原始出處：
（British Journal of Cancer）,，doi:10.1038/sj.bjc.6604319,，D Sliva, V Slivova
Phellinus linteus suppresses growth, angiogenesis and invasive behaviour of breast cancer cells through the inhibition of AKT signalling
D Sliva1,2,3, A Jedinak1, J Kawasaki1, K Harvey1 and V Slivova1
1Cancer Research Laboratory, Methodist Research Institute, 1800 N Capitol Ave, E504, Indianapolis, IN 46202, USA
2Department of Medicine, Indiana University, Indianapolis, IN, USA
3Indiana University Simon Cancer Center, School of Medicine, Indiana University, Indianapolis, IN, USA
The antitumour activity of a medicinal mushroom Phellinus linteus (PL), through the stimulation of immune system or the induction of apoptosis, has been recently described. However, the molecular mechanisms responsible for the inhibition of invasive behaviour of cancer cells remain to be addressed. In the present study, we demonstrate that PL inhibits proliferation (anchorage-dependent growth) as well as colony formation (anchorage-independent growth) of highly invasive human breast cancer cells. The growth inhibition of MDA-MB-231 cells is mediated by the cell cycle arrest at S phase through the upregulation of p27Kip1 expression. Phellinus linteus also suppressed invasive behaviour of MDA-MB-231 cells by the inhibition of cell adhesion, cell migration and cell invasion through the suppression of secretion of urokinase-plasminogen activator from breast cancer cells. In addition, PL markedly inhibited the early event in angiogenesis, capillary morphogenesis of the human aortic endothelial cells, through the downregulation of secretion of vascular endothelial growth factor from MDA-MB-231 cells. These effects are mediated by the inhibition of serine-threonine kinase AKT signalling, because PL suppressed phosphorylation of AKT at Thr308 and Ser473 in breast cancer cells. Taken together, our study suggests potential therapeutic effect of PL against invasive breast cancer.
