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NF-kappaB阻塞和瘤性Ras触发了侵袭性人类表皮瘤

Maya Dajee¹, Mirella Lazarov, Jennifer Y Zhang

¹Veterans Affairs Palo Alto Healthcare System and the Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California 94305, USA.

|February 7, 2003

概括

核因子kappa B (NF-kappaB) 和瘤性Ras通常会在人类表皮细胞中阻止细胞循环. 用致癌的Ras阻断NF-kappaB可以导致状细胞癌.

科学领域:

在瘤学瘤学.
细胞生物学细胞生物学
皮肤病学皮肤病学

背景情况:

核因子NF-kappaB和瘤性Ras调节表皮中的细胞增殖,这是人类癌症的常见部位.
虽然它们与小鼠状细胞癌有关,但它们在人类表皮细胞中的确切作用尚不清楚.
针对Ras和NF-kappaB通路的治疗方法正在开发中,用于人类癌症治疗.

研究的目的:

研究改变正常人表皮细胞中NF-kappaB和瘤性Ras功能的影响.
确定这些因素影响细胞循环停止和瘤发生的机制.
评估NF-kappaB阻塞促进Ras诱导的恶性转变的潜力.

主要方法:

使用了正常的人类表皮细胞.
研究了NF-kappaB和瘤原Ras对细胞循环停止的影响.
检查了IkappaBalpha在调节Ras诱导的增长停止中的作用.
评估了人体细胞瘤发生的依赖性对拉米宁5和α6β4整合素.

主要成果:

发现NF-kappaB和瘤性Ras都会在正常的人类表皮细胞中触发细胞循环停止.
瘤性Ras诱导的生长停止可以通过IkappaBalpha介导的NF-kappaB阻断来克服.
这种阻塞,与瘤性Ras结合,产生了类似状细胞癌的恶性人体表皮组织.
在这种情况下,人类细胞瘤发生取决于拉米宁5和α6β4整合蛋白.

结论:

NF-kappaB和瘤性Ras作为人类表皮细胞循环控制的关键调节剂.
伊卡帕巴尔法可以绕过致癌性Ras.的增长抑制信号.
拉斯和NF-kappaB阻断的联合作用可以诱导侵袭性人类瘤,突出潜在的治疗脆弱性.

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