美国密歇根大学科研人员最新研究发现，在胰腺癌细胞中，一种名为ATDC的基因表达水平是正常胰腺细胞中表达水平的20倍，而且这种基因能增强胰腺癌细胞对现有疗法的耐受性。
研究人员在3月刊的《癌细胞》杂志上介绍说，他们将ATDC基因充分表达或被抑制的胰腺肿瘤细胞分别注入两组实验鼠体内。60天后，ATDC基因充分表达组的实验鼠体内胰腺肿瘤增大，良性向恶化发展，并出现扩散；而对照组实验鼠只有很小的肿瘤生长迹象。研究人员认为，这表明ATDC基因促进了胰腺肿瘤细胞的生长和恶性病变。
研究认为，这种基因在膀胱癌、肺癌的发展过程中可能也扮演了某种角色。
负责这项研究的迪亚纳·西梅奥内说，ATDC基因不仅导致胰腺癌细胞生长更快、更富有攻击性，而且会增加其对化疗和放疗的耐受性。如果开发出以这种基因为靶向的药物或疗法，或许能增强现有化疗、放疗对胰腺癌的治疗效果。（生物谷Bioon.com）
生物谷推荐原始出处：
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.
