美國密歇根大學科研人員最新研究發(fā)現(xiàn)，在胰腺癌細胞中,，一種名為ATDC的基因表達水平是正常胰腺細胞中表達水平的20倍,，而且這種基因能增強胰腺癌細胞對現(xiàn)有療法的耐受性。
研究人員在3月刊的《癌細胞》雜志上介紹說,，他們將ATDC基因充分表達或被抑制的胰腺腫瘤細胞分別注入兩組實驗鼠體內,。60天后，ATDC基因充分表達組的實驗鼠體內胰腺腫瘤增大,，良性向惡化發(fā)展,，并出現(xiàn)擴散；而對照組實驗鼠只有很小的腫瘤生長跡象,。研究人員認為,，這表明ATDC基因促進了胰腺腫瘤細胞的生長和惡性病變。
研究認為,，這種基因在膀胱癌,、肺癌的發(fā)展過程中可能也扮演了某種角色。
負責這項研究的迪亞納·西梅奧內說,，ATDC基因不僅導致胰腺癌細胞生長更快,、更富有攻擊性，而且會增加其對化療和放療的耐受性,。如果開發(fā)出以這種基因為靶向的藥物或療法，或許能增強現(xiàn)有化療,、放療對胰腺癌的治療效果,。（生物谷Bioon.com）
生物谷推薦原始出處：
Cancer Cell, 3 March 2009 doi:10.1016/j.ccr.2009.01.018
Oncogenic Function of ATDC in Pancreatic Cancer through Wnt Pathway Activation and -Catenin Stabilization
Lidong Wang1,David G. Heidt1,Cheong J. Lee1,Huibin Yang1,Craig D. Logsdon5,Lizhi Zhang6,Eric R. Fearon3,4,7,Mats Ljungman2andDiane M. Simeone1,8,,
1 Department of Surgery, University of Michigan Medical Center, Ann Arbor, MI 48109, USA
2 Department of Radiation Oncology, University of Michigan Medical Center, Ann Arbor, MI 48109, USA
3 Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI 48109, USA
4 Department of Pathology, University of Michigan Medical Center, Ann Arbor, MI 48109, USA
5 Department of Cancer Biology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA
6 Department of Pathology, Mayo Clinic, Rochester, MN 55905, USA
7 Department of Human Genetics, University of Michigan, Ann Arbor, MI 48109, USA
8 Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA
Pancreatic cancer is a deadly disease characterized by late diagnosis and resistance to therapy. Much progress has been made in defining gene defects in pancreatic cancer, but a full accounting of its molecular pathogenesis remains to be provided. Here, we show that expression of the ataxia-telangiectasia group D complementing gene (ATDC), also called TRIM29, is elevated in most invasive pancreatic cancers and pancreatic cancer precursor lesions. ATDC promoted cancer cell proliferation invitro and enhanced tumor growth and metastasis invivo. ATDC expression correlated with elevated β-catenin levels in pancreatic cancer, and β-catenin function was required for ATDC's oncogenic effects. ATDC was found to stabilize β-catenin via ATDC-induced effects on the Disheveled-2 protein, a negative regulator of glycogen synthase kinase 3 in the Wnt/β-catenin signaling pathway.
