英國(guó)一項(xiàng)最新研究發(fā)現(xiàn),，一種特殊的“激酶抑制劑”可以幫助健康細(xì)胞和癌細(xì)胞進(jìn)行“對(duì)話”，最終“說服”癌細(xì)胞回到正常細(xì)胞狀態(tài),。
來(lái)自英國(guó)曼徹斯特大學(xué)和索爾福德大學(xué)的研究人員在新一期《英國(guó)癌癥雜志》上報(bào)告說,，他們?cè)谠嚬苤谢旌吓囵B(yǎng)健康細(xì)胞和癌細(xì)胞，當(dāng)加入這種“激酶抑制劑”后,，健康細(xì)胞和癌細(xì)胞的表面建立起了信息傳遞通道,，隨后健康細(xì)胞似乎“控制”了癌細(xì)胞的生長(zhǎng)，癌細(xì)胞最終停止無(wú)序繁殖擴(kuò)散,，其行為變得和正常細(xì)胞一樣,。
一般情況下，人體中各種細(xì)胞都有序地生長(zhǎng),、繁殖和死亡,，但發(fā)生病變的癌細(xì)胞常常會(huì)失去控制地進(jìn)行分化和繁殖。
研究人員說,，即使在移除這種“激酶抑制劑”后,，健康細(xì)胞和癌細(xì)胞間已建立的交流通道仍然會(huì)保持通暢。再加上這種“激酶抑制劑”沒有毒性,，今后可以在此基礎(chǔ)上開發(fā)出快捷高效并且副作用小的癌癥療法,。
不過，研究也顯示,，如果向只含有癌細(xì)胞的試管中加入這種物質(zhì),，則基本沒有效果,。這說明需要有大量的健康細(xì)胞來(lái)進(jìn)行“說服”癌細(xì)胞的工作。
就一般情況下人體中健康細(xì)胞和癌細(xì)胞的比例而言,，這種物質(zhì)可以起到良好的治療效果,。（生物谷Bioon.com）
生物谷推薦原始出處：
British Journal of Cancer (2009) 101, 829–839. doi:10.1038/sj.bjc.6605208
Analogues of Y27632 increase gap junction communication and suppress the formation of transformed NIH3T3 colonies
L Hampson1, X T He1, A W Oliver1, J A Hadfield2, T Kemp2, J Butler2, A McGown2, H C Kitchener1 and I N Hampson1
1University of Manchester School of Cancer Studies and Imaging Science, Gynaecological Oncology Laboratories, St Mary's Hospital, Hathersage Road, Manchester M13 OJH, UK
2Centre for Molecular Drug Design, Kidscan Laboratories, Cockcroft Building, University of Salford, Manchester M5 4WT, UK
background: Constitutive activation of RhoA-dependent RhoA kinase (ROCK) signalling is known to promote cellular transformation and the ROCK inhibitor Y-27632 has the ability to suppress focus formation of RhoA transformed NIH3T3 cells.
methods: Sixty-four novel structural analogues of Y27632 were synthesised and tested for their ability to persistently inhibit the transformation of NIH3T3 cells by Rho guanidine exchange factor 16 (ARHGEF16) or Ras. In vitro kinase inhibitor profiling, co-culture of transformed cells with non-transformed cells and a novel Lucifer yellow/PKH67 dye transfer method were used to investigate their mode of action.
results: Four Y27632 analogues inhibited transformed focus formation that persisted when the compound was withdrawn. No toxicity was observed against either transformed or non-transformed cells and the effect was dependent on co-culture of these two cell types. In vitro kinase inhibitor profiling indicated that these compounds had reduced activity against ROCK compared with Y27632, targeting instead Aurora A (AURKA), p38 (MAPK14) and Hgk (MAP4K4). Dye transfer analysis showed they increased gap junction intercellular communication (GJIC) between transformed and non-transformed cells.
conclusions: These data are the first to suggest that transient blockade of specific kinases can induce a persistent inhibition of non-contact inhibited transformed colony formation and can also remove pre-formed colonies. These effects could potentially be mediated by the observed increase in GJIC between transformed and non-transformed cells. Selection of kinase inhibitors with this property may thus provide a novel strategy for cancer chemoprevention.
