Depletion of Jab 1 inhibits proliferation of pancreatic cancer cell lines
Depletion of Jab 1 inhibits proliferation of pancreatic cancer cell lines
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DOI：
10.1016/j.febslet.2006.09.042
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发表时间：
2006-10-30
期刊：
影响因子：
3.5
通讯作者：
Kato, Jun-ya
中科院分区：
文献类型：
--
作者：
Fukumoto, Akihisa;Tomoda, Kiichiro;Kato, Jun-ya
在许多人类癌症中观察到 Jab1 过度表达，但其生理意义仍有待研究。我们通过 RNA 干扰降低了胰腺癌细胞系 MIA PaCa-2 和 PANC-1 中 Jab1 的表达水平，发现无论肿瘤抑制因子 p53 的基因型如何，Jab1 敲低都会导致细胞增殖受损并增强细胞凋亡。通过引入 siRNA 抗性小鼠 Jab1 cDNA，可以挽救这种生长抑制。 Jab1 敲低的细胞表达更高水平的 c-myc，额外去除 c-myc 可将细胞从 Jab1 敲低介导的生长抑制中拯救出来。因此，Jab1 过度表达有助于胰腺癌细胞增殖和存活。 Jab1 可能成为癌症治疗的新靶点。 (c) 2006 年欧洲生化学会联合会。由 Elsevier B.V. 出版。保留所有权利。
Jab1 overexpression is observed in many human cancers, but its physiological significance remains to be investigated. We reduced the level of Jab1 expression in pancreatic cancer cell lines, MIA PaCa-2 and PANC-1 by the RNA interference and found that Jab1-knockdown resulted in impaired cell proliferation and enhanced apoptosis regardless of the genotype of the tumor suppressor p53. This growth inhibition was rescued by the introduction of siRNA-resistant mouse Jab1 cDNA. Jab1-knocked-down cells expressed a higher level of c-myc, and additional depletion of c-myc rescued cells from Jab1-knockdown-mediated growth suppression. Thus, Jab1 overexpression contributes to pancreatic cancer cell proliferation and survival. Jab1 could be a novel target in cancer therapy. (c) 2006 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.