美國(guó)密歇根大學(xué)科研人員最新研究發(fā)現(xiàn),，在胰腺癌細(xì)胞中,，一種名為ATDC的基因表達(dá)水平是正常胰腺細(xì)胞中表達(dá)水平的20倍,，而且這種基因能增強(qiáng)胰腺癌細(xì)胞對(duì)現(xiàn)有療法的耐受性。
研究人員在3月刊的《癌細(xì)胞》雜志上介紹說(shuō),，他們將ATDC基因充分表達(dá)或被抑制的胰腺腫瘤細(xì)胞分別注入兩組實(shí)驗(yàn)鼠體內(nèi),。60天后，ATDC基因充分表達(dá)組的實(shí)驗(yàn)鼠體內(nèi)胰腺腫瘤增大,，良性向惡化發(fā)展,，并出現(xiàn)擴(kuò)散；而對(duì)照組實(shí)驗(yàn)鼠只有很小的腫瘤生長(zhǎng)跡象,。研究人員認(rèn)為,，這表明ATDC基因促進(jìn)了胰腺腫瘤細(xì)胞的生長(zhǎng)和惡性病變。
研究認(rèn)為,，這種基因在膀胱癌,、肺癌的發(fā)展過(guò)程中可能也扮演了某種角色。
負(fù)責(zé)這項(xiàng)研究的迪亞納·西梅奧內(nèi)說(shuō),，ATDC基因不僅導(dǎo)致胰腺癌細(xì)胞生長(zhǎng)更快,、更富有攻擊性，而且會(huì)增加其對(duì)化療和放療的耐受性,。如果開發(fā)出以這種基因?yàn)榘邢虻乃幬锘虔煼?，或許能增強(qiáng)現(xiàn)有化療、放療對(duì)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.
