Nuclear factor-[kappa]B signaling pathway is involved in phospholipase C[epsilon]-regulated proliferation in human renal cell carcinoma cells

• Published in: Molecular and cellular biochemistry 2014-04, Vol.389 (1-2), p.265
• Main Authors: Du, Hong-fei, Ou, Li-ping, Song, Xue-dong, Fan, Yan-ru, Yang, Xue, Tan, Bing, Quan, Zhen, Luo, Chun-li, Wu, Xiao-hou
• Format: Article
• Language: English
• Subjects: Cells; Kidney diseases; Signal transduction
• ISSN: 0300-8177; 1573-4919
• DOI: 10.1007/s11010-013-1948-4

Phospholipase C[straight epsilon] (PLC[straight epsilon]), a downstream effector of small GTPase superfamily, has been identified to play a crucial role in tumorigenesis. Previously, our studies have showed that PLC[straight epsilon] promotes proliferation of renal cell carcinoma (RCC) cells. However, the molecular mechanisms by which PLC[straight epsilon] enhances the survival phenotype of RCC cells are still not fully instructed. In the present study, we first demonstrated that PLC[straight epsilon] was highly expressed and had a close correlation with Ki67 protein expression in RCC tissue samples. Further, we found that downregulation of PLC[straight epsilon] expression repressed growth and induced apoptosis in RCC cells. In addition, we reported a mechanism by which knockdown of PLC[straight epsilon] gene potently suppressed the nuclear factor kappa (NF-[kappa]B) signaling pathway through action on inhibitor of [kappa]B kinase. Moreover, silencing PLC[straight epsilon] gene decreased vascular endothelial growth factor (VEGF) expression, which was a downstream growth factor of NF-[kappa]B signaling pathway. Finally, downregulation of VEGF was severely enhanced by treatment cells with NF-[kappa]B specific inhibitor BAY11-7028 in PLC[straight epsilon] knockdown cells. Taken together, these findings suggest that PLC[straight epsilon] promotes RCC cell growth via NF-[kappa]B-mediated upregulation of VEGF.[PUBLICATION ABSTRACT]