近日,，國際著名雜志Cancer Research上刊登了韓國成均館大學醫(yī)學院研究者的最新研究成果“MET Signaling Regulates Glioblastoma Stem Cells”,，文章中,，研究者揭示了間葉組織-表皮組織轉變（MET）信號路徑可以調節(jié)膠質母細胞瘤干細胞,。
多形性膠質母細胞瘤（GBM）是一種常見的致死率極高的腦部腫瘤,，是神經膠質瘤的一種,。這種腦瘤具有高琴潤性，可以大范圍的進行轉移,，治療后復發(fā)率較高,。
GBM具有極高的致瘤性，可以通過膠質母細胞瘤干細胞（GSCs）進行自我更新,，最終使得腫瘤擴散以及產生耐藥。目前調節(jié)膠質母細胞瘤干細胞的路徑非常有限,。眾所周知,，MET酪氨酸激酶在很多癌癥包括GBM中可以刺激腫瘤生存、增殖以及擴散,。
在研究報告中,，研究者Do-Hyun Nam指出，他們在人類初始GBM樣品中發(fā)現(xiàn)了可以表達高水平MET的細胞特殊部分,，這些特殊的細胞部分可以優(yōu)先地集中于人類GBM活檢組織樣品的血管周圍區(qū)域,，并且具有高度獨立性、致瘤性以及對放療產生耐受性,。
體外和體內實驗中,，研究者發(fā)現(xiàn)，在膠質母細胞瘤干細胞抑制MET信號路徑可以破壞腫瘤的生長和其擴散,，因此研究者表示,，MET的激活需要膠質母細胞瘤干細胞。
因此研究者的研究結果表明了,，在多形性膠質母細胞瘤中MET的激活是癌癥干細胞表型的功能要素,，其或許會成為未來治療的一個潛在靶點。（生物谷Bioon.com）
doi:10.1158/0008-5472.CAN-11-3760
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PMID:
MET Signaling Regulates Glioblastoma Stem Cells
Kyeung Min Joo1,3, Juyoun Jin1,2, Eunhee Kim5, Kang Ho Kim1,2, Yonghyun Kim1, Bong Gu Kang1,2, Youn-Jung Kang1,2, Justin D. Lathia5, Kwang Ho Cheong6, Paul H. Song6, Hyunggee Kim4, Ho Jun Seol1,2, Doo-Sik Kong2, Jung-Il Lee2, Jeremy N. Rich5, Jeongwu Lee5, and Do-Hyun Nam1,2
Glioblastomas multiforme (GBM) contain highly tumorigenic, self-renewing populations of stem/initiating cells [glioblastoma stem cells (GSC)] that contribute to tumor propagation and treatment resistance. However, our knowledge of the specific signaling pathways that regulate GSCs is limited. The MET tyrosine kinase is known to stimulate the survival, proliferation, and invasion of various cancers including GBM. Here, we identified a distinct fraction of cells expressing a high level of MET in human primary GBM specimens that were preferentially localized in perivascular regions of human GBM biopsy tissues and were found to be highly clonogenic, tumorigenic, and resistant to radiation. Inhibition of MET signaling in GSCs disrupted tumor growth and invasiveness both in vitro and in vivo, suggesting that MET activation is required for GSCs. Together, our findings indicate that MET activation in GBM is a functional requisite for the cancer stem cell phenotype and a promising therapeutic target. Cancer Res; 72(15); 3828–38. ©2012 AACR.
