據(jù)韓聯(lián)社報(bào)道，位于韓國光矯（地名）科技園的醫(yī)藥生物融合研究組日前談稱,，其發(fā)現(xiàn)了導(dǎo)致肺癌的因子AIMP2-DX2,。
該組稱，AIMP2-DX2是AIMP2蛋白質(zhì)的一種變異體,，試驗(yàn)結(jié)果顯示,，注入AIMP2-DX2的18只白鼠中有14只患得肺癌，而對(duì)另外12只白鼠注入其他致癌物質(zhì)的結(jié)果,，只有4只患得肺癌,，對(duì)已患肺癌的白鼠進(jìn)行遏制AIMP2-DX2的結(jié)果，病情得到有效控制,。
研究組對(duì)三星醫(yī)療院,、慶北大學(xué)附屬醫(yī)院和美國Rosewell Park Cancel Institute(Buffalo, N.Y.)的97名肺癌患者進(jìn)行了調(diào)研，發(fā)現(xiàn)肺癌的進(jìn)展與AIMP2-DX2的增長密切相關(guān),，證實(shí)了AIMP2-DX2是治療肺癌的重要目標(biāo)因子,。
該項(xiàng)研究結(jié)果已于本月1日刊登在《公共科學(xué)圖書館遺傳學(xué)（PLoS Genetics）》雜志上。（生物谷Bioon.com）
生物谷推薦原文出處：
PLoS Genet 7(3): e1001351. doi:10.1371/journal.pgen.1001351
Cancer-Associated Splicing Variant of Tumor Suppressor AIMP2/p38: Pathological Implication in Tumorigenesis
Jin Woo Choi1, Dae Gyu Kim1, Al-Eum Lee1, Hye Rim Kim1, Jin Young Lee1, Nam Hoon Kwon1, Young Kee Shin2, Soon-Kyung Hwang3, Seung-Hee Chang3, Myung-Haing Cho3, Yoon-La Choi4, Jhingook Kim5, Seung Hyun Oh6, Bora Kim6, Soo-Youl Kim6, Hyo-Sung Jeon7, Jae Yong Park8, Hyunseok Peter Kang9, Bum Joon Park10, Jung Min Han1,11, Sunghoon Kim1,11*
Abstract
Although ARS-interacting multifunctional protein 2 (AIMP2, also named as MSC p38) was first found as a component for a macromolecular tRNA synthetase complex, it was recently discovered to dissociate from the complex and work as a potent tumor suppressor. Upon DNA damage, AIMP2 promotes apoptosis through the protective interaction with p53. However, it was not demonstrated whether AIMP2 was indeed pathologically linked to human cancer. In this work, we found that a splicing variant of AIMP2 lacking exon 2 (AIMP2-DX2) is highly expressed by alternative splicing in human lung cancer cells and patient's tissues. AIMP2-DX2 compromised pro-apoptotic activity of normal AIMP2 through the competitive binding to p53. The cells with higher level of AIMP2-DX2 showed higher propensity to form anchorage-independent colonies and increased resistance to cell death. Mice constitutively expressing this variant showed increased susceptibility to carcinogen-induced lung tumorigenesis. The expression ratio of AIMP2-DX2 to normal AIMP2 was increased according to lung cancer stage and showed a positive correlation with the survival of patients. Thus, this work identified an oncogenic splicing variant of a tumor suppressor, AIMP2/p38, and suggests its potential for anti-cancer target.
