2014年2月13日 訊 /生物谷BIOON/ --正常情況下，胰臟星狀細胞(Pancreatic stellate cells)可以幫助進行組織修復，但是近日一項來自倫敦王后大學研究人員的研究結果顯示，這種胰臟星狀細胞有時候也可以幫助胰腺癌細胞的生長，並且可以在大腦和乳腺癌個體中劫持機體的健康細胞，相關研究成果刊登於國際雜誌EMBO Molecular Medicine上。
文章中，研究者也揭示了阻斷胰臟星狀細胞行為的過程，研究者發現癌症細胞可以使用一種名為纖維母細胞生長因子受體（FGFR）的蛋白質來攔截星形細胞，從而迫使星形細胞來幫助腫瘤細胞生長。正常情況下，纖維母細胞生長因子可以通過結合到細胞表面的受體來激活星形細胞，而且研究者發現FGFR可以直接進入到細胞核中控制並且驅動星形細胞增殖以及同癌細胞進行信號交流。這種核轉位行為之前僅僅在腦癌和乳腺癌中發現過。
當阻斷FGFR的活性並且抑制星形細胞被「劫持」就可以完全阻斷癌細胞生長和侵襲，胰腺癌細胞通常會表現出對傳統化療的耐受性，部分原因是癌症間質可以抑制療法對腫瘤細胞作用，下一步研究人員將調查FGFR進入細胞核後對星形細胞帶來的改變，目的在於揭示星形細胞如何促進癌細胞生長。
最後研究者Maggie Blanks表示，這項研究會我們基於傳統療法開通新型抵禦癌症的療法提供了一定的思路，未來我們將通過不懈的努力定能開發出改善胰腺癌的新型療法。（生物谷Bioon.com）
Nuclear translocation of FGFR1 and FGF2 in pancreatic stellate cells facilitates pancreatic cancer cell invasion
Stacey J Coleman, Athina‐Myrto Chioni, Mohammed Ghallab, Rhys K Anderson, Nicholas R Lemoine, Hemant M Kocher, Richard P Grose
Pancreatic cancer is characterised by desmoplasia, driven by activated pancreatic stellate cells (PSCs). Over‐expression of FGFs and their receptors is a feature of pancreatic cancer and correlates with poor prognosis, but whether their expression impacts on PSCs is unclear. At the invasive front of human pancreatic cancer, FGF2 and FGFR1 localise to the nucleus in activated PSCs but not cancer cells. In vitro, inhibiting FGFR1 and FGF2 in PSCs, using RNAi or chemical inhibition, resulted in significantly reduced cell proliferation, which was not seen in cancer cells. In physiomimetic organotypic co‐cultures, FGFR inhibition prevented PSC as well as cancer cell invasion. FGFR inhibition resulted in cytoplasmic localisation of FGFR1 and FGF2, in contrast to vehicle‐treated conditions where PSCs with nuclear FGFR1 and FGF2 led cancer cells to invade the underlying extra‐cellular matrix. Strikingly, abrogation of nuclear FGFR1 and FGF2 in PSCs abolished cancer cell invasion. These findings suggest a novel therapeutic approach, where preventing nuclear FGF/FGFR mediated proliferation and invasion in PSCs leads to disruption of the tumour microenvironment, preventing pancreatic cancer cell invasion.