Id1 和 NF-κB 促进了 CD133+ 和 BMI-1+ 角质形成细胞的生成，并促进了小鼠异种移植肿瘤的生长。
Id1 and NF-κB promote the generation of CD133+ and BMI-1+ keratinocytes and the growth of xenograft tumors in mice.
机构信息
Department of Oncology of Union Hospital, Institute of Immunotherapy, Fujian Medical University, Fuzhou, P.R. China.
Department of Otolaryngology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangdong, P.R. China.
出版信息
Int J Oncol. 2014 May;44(5):1481-9. doi: 10.3892/ijo.2014.2309. Epub 2014 Feb 21.
Id1 and NF-κB are highly expressed in oral squamous cell carcinoma (OSCC). Whether they have a synergistic role in the carcinogenesis of OSCC is unclear. The current study was designed to demonstrate the synergy of both Id1 and NF-κB in the underlying disease mechanisms of OSCC using in vitro and in vivo animal models. Id1 and NF-κB strengthened the expression of both CD133 and BMI-1 in OSCC cell cultures. CD133(+) and BMI-1(+) keratinocytes from OSCC tissues and cell cultures initiated the growth of xenograft tumors in SCID/Beige mice. Id1 and NF-κB regulate the expression of CD133 and BMI-1 in an additive or synergistic manner in OSCC, which is associated with the generation of naïve and self-renewable keratinocytes and initiate the growth of xenograft tumors in vivo.
Id1 和 NF-κB 在口腔鳞状细胞癌（OSCC）中高度表达。它们在 OSCC 的发生机制中是否具有协同作用尚不清楚。本研究旨在使用体外和体内动物模型证明 Id1 和 NF-κB 在 OSCC 潜在疾病机制中的协同作用。Id1 和 NF-κB 增强了 OSCC 细胞培养物中 CD133 和 BMI-1 的表达。来自 OSCC 组织和细胞培养物的 CD133(+)和 BMI-1(+)角质形成细胞启动了 SCID/Beige 小鼠异种移植瘤的生长。Id1 和 NF-κB 以累加或协同的方式调节 OSCC 中 CD133 和 BMI-1 的表达，这与幼稚和自我更新的角质形成细胞的产生有关，并在体内启动异种移植瘤的生长。
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