Jeang Kuan-Teh
Oncotarget. 2010 Oct;1(6):453-456. doi: 10.18632/oncotarget.179.
The mechanism of HTLV-1 transformation of cells to Adult T cell leukemia (ATL) remains not fully understood. Currently, the viral Tax oncoprotein is known to be required to initiate transformation. Emerging evidence suggests that Tax is not needed to maintain the transformed ATL phenotype. Recent studies have shown that HTLV-1 transformed cells show deregulated expression of cellular microRNAs (miRNAs). Here we discuss the possibility that early ATL cells are Tax-oncogene-addicted while late ATL cells are oncogenic microRNA (oncomiR) - addicted. The potential utility of interrupting oncomiR addiction as a cancer treatment is broached.
人嗜T淋巴细胞病毒1型(HTLV-1)将细胞转化为成人T细胞白血病(ATL)的机制仍未完全明确。目前已知病毒Tax癌蛋白是启动转化所必需的。新出现的证据表明,维持ATL转化表型并不需要Tax。最近的研究表明,HTLV-1转化细胞表现出细胞微小RNA(miRNA)表达失调。在此,我们探讨了早期ATL细胞对Tax癌基因成瘾而晚期ATL细胞对致癌微小RNA(致癌miR)成瘾的可能性。文中还提及了将中断致癌miR成瘾作为癌症治疗手段的潜在效用。