Wang Xuguang, Chen Zhe
Department of Thoracic Surgery, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
Oncol Res. 2016;24(4):271-7. doi: 10.3727/096504016X14666990347473.
Cullin 4B (CUL4B), a scaffold protein that assembles CRL4B ubiquitin ligase complexes, was found to be overexpressed in many types of tumors. However, the expression pattern and role of CUL4B in non-small cell lung cancer (NSCLC) remain largely unknown. Therefore, in the present study, we investigated the role of CUL4B in NSCLC, and the underlying mechanism was also explored. Our results showed that CUL4B was highly expressed in NSCLC cell lines. Silencing CUL4B obviously inhibited proliferation and migration/invasion of NSCLC cells, and it also suppressed the epithelial-mesenchymal transition (EMT) progress in NSCLC cells. Furthermore, knockdown of CUL4B significantly inhibited the expression of β-catenin, cyclin D1, and c-Myc in NSCLC cells. Taken together, these results suggest that knockdown of CUL4B inhibited the proliferation and invasion through suppressing the Wnt/β-catenin signaling pathway in NSCLC cells. Therefore, CUL4B may represent a novel therapeutic target for the treatment of NSCLC.
Cullin 4B(CUL4B)是一种组装CRL4B泛素连接酶复合物的支架蛋白,在多种肿瘤中均有过表达。然而,CUL4B在非小细胞肺癌(NSCLC)中的表达模式和作用仍不清楚。因此,在本研究中,我们探究了CUL4B在NSCLC中的作用,并对其潜在机制进行了探索。我们的结果显示,CUL4B在NSCLC细胞系中高表达。沉默CUL4B明显抑制了NSCLC细胞的增殖、迁移和侵袭,同时也抑制了NSCLC细胞中的上皮-间质转化(EMT)进程。此外,敲低CUL4B显著抑制了NSCLC细胞中β-连环蛋白、细胞周期蛋白D1和c-Myc的表达。综上所述,这些结果表明敲低CUL4B通过抑制NSCLC细胞中的Wnt/β-连环蛋白信号通路来抑制其增殖和侵袭。因此,CUL4B可能是治疗NSCLC的一个新的治疗靶点。