Chen Xin, Hu Yuanyuan, Wang Shuo, Sun Xiulian
Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, P. R. China.
China National Clinical Research Center for Neurological Diseases, Beijing, P. R. China.
Oncotarget. 2017 Feb 14;8(7):12003-12012. doi: 10.18632/oncotarget.14479.
Nuclear factor-kappaB (NF-κB) has a vital role in cell survival and inhibition of NF-κB had proven to be an efficient therapeutic pathway for various cancers though little is known about the underlying mechanism. Previously we identified regulator of calcineurin 1 (RCAN1) as an endogenous inhibitor of NF-κB signaling pathway in lymphoma. In the present study, we have solid data to show that RCAN1 can inhibit the nuclear translocation of NF-κB protein then affect the activity of NF-κB signaling pathway in glioma cells. Overexpression of RCAN1 markedly reduced glioma cells viability. We further found that the suppressing glioma cell growth was closely related to the pro-apoptosis effect, not by inhibiting proliferation by the arrest of cell cycle. Our study implicated a novel therapeutic approach for glioma by RCAN1 through inhibition of NF-κB signaling.
核因子-κB（NF-κB）在细胞存活中起着至关重要的作用，尽管对其潜在机制知之甚少，但抑制NF-κB已被证明是治疗多种癌症的有效途径。此前我们鉴定出钙调神经磷酸酶1调节因子（RCAN1）是淋巴瘤中NF-κB信号通路的内源性抑制剂。在本研究中，我们有确凿的数据表明，RCAN1可抑制NF-κB蛋白的核转位，进而影响胶质瘤细胞中NF-κB信号通路的活性。RCAN1的过表达显著降低了胶质瘤细胞的活力。我们进一步发现，抑制胶质瘤细胞生长与促凋亡作用密切相关，而非通过细胞周期阻滞抑制增殖。我们的研究表明，RCAN1通过抑制NF-κB信号传导为胶质瘤提供了一种新的治疗方法。
