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5月31日，瑞典卡羅林斯卡醫(yī)學(xué)院宣布發(fā)現(xiàn)了胰腺癌細(xì)胞變化的新機(jī)理，這將有助于胰腺癌的早期診斷。
根據(jù)現(xiàn)有研究成果，胰腺癌與以下兩種特殊的細(xì)胞結(jié)構(gòu)變化有關(guān)：RAS致癌基因發(fā)生突變；大量分子信號(hào)是按照一種“刺猬”式信號(hào)傳遞的。
瑞典卡羅林斯卡醫(yī)學(xué)院的研究人員在對(duì)老鼠實(shí)驗(yàn)后，發(fā)現(xiàn)了RAS基因和“刺猬”式信號(hào)傳遞相互作用的機(jī)理。當(dāng)RAS基因被激活時(shí)，腫瘤細(xì)胞就會(huì)分泌SHH，這種物質(zhì)會(huì)引發(fā)“刺猬”式信號(hào)傳遞活動(dòng)，同時(shí)阻止腫瘤細(xì)胞對(duì)這種信號(hào)做出反應(yīng)。整個(gè)過(guò)程分為兩個(gè)階段：*階段在“刺猬”式信號(hào)刺激下，腫瘤細(xì)胞周圍的細(xì)胞會(huì)迅速生長(zhǎng)，而腫瘤細(xì)胞在SHH保護(hù)下處于安全狀態(tài)；第二階段當(dāng)SHH的作用消失時(shí)，腫瘤細(xì)胞在“刺猬”式信號(hào)的刺激下加速生長(zhǎng)，腫瘤開(kāi)始逐漸惡化，直至形成癌癥。
這一成果發(fā)表在新一期《自然·結(jié)構(gòu)與分子生物學(xué)》雜志上。
上海勁馬生物（）推薦原文出處：
Nature Structural & Molecular Biology doi:10.1038/nsmb.1833
DYRK1B-dependent autocrine-to-paracrine shift of Hedgehog signaling by mutant RAS
Matthias Lauth1,4, ?sa Bergstr?m1, Takashi Shimokawa1, Ulrica Tostar1, Qianren Jin1, Volker Fendrich2, Carmen Guerra3, Mariano Barbacid3 & Rune Toftg?rd1
Synergism between the RAS and Hedgehog （HH） pathways has been suggested for carcinogenesis in the pancreas, lung and colon. We investigated the molecular cross-talk between RAS and HH signaling and found that, although mutant RAS induces or enhances SHH expression and favors paracrine HH signaling, it antagonizes autocrine HH signal transduction. Activated RAS can be found in primary cilia, the central organelle of HH signal transduction, but functions in a cilium-independent manner and interferes with Gli2 function and Gli3 processing. In addition, the cell-autonomous negative regulation of HH signal transduction involves the RAS effector molecule dual specificity tyrosine phosphorylated and regulated kinase 1B （DYRK1B）. In line with a redirection of autocrine toward paracrine HH signaling by a KRAS-DYRK1B network, we find high levels of GLI1 expression restricted to the stromal compartment and not to SHH-expressing tumor cells in human pancreatic adenocarcinoma.
