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Retracted : Role of RKIP in human hepatic stellate cell proliferation, invasion, and metastasis
Author(s) -
Huang Quanfang,
Wei Jinbin,
Wei Ling,
Zhang Xiaolin,
Bai Facheng,
Wen Shujuan,
Wei Yuanyuan,
Tan Shimei,
Lu Zhongpeng,
Lin Xing
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27904
Subject(s) - mapk/erk pathway , hepatic stellate cell , microbiology and biotechnology , small interfering rna , transfection , cell growth , signal transduction , chemistry , cell cycle , kinase , apoptosis , protein kinase a , cancer research , biology , cell culture , endocrinology , biochemistry , genetics
The purpose of this study was to investigate the effect of Raf kinase inhibitor protein (RKIP) on the growth, apoptosis, invasion, and metastasis of human hepatic stellate cell line (LX‐2). A recombinant plasmid (pcDNA3.1‐RKIP) or RKIP‐targeting small interfering RNA (siRNA) vector (siRNA‐RKIP) was transfected into LX‐2 cells to interfere with the RKIP expression. The results demonstrated that increased RKIP expression significantly reduced cell viability, clonogenic growth, and invasion. Further, it promoted cell apoptosis and induced cell cycle arrest in the G1 phase. Overexpression of RKIP led to inactivation of LX‐2 cells, as evidenced by the decrease in the expression levels of collagen I and α‐smooth muscle actin (α‐SMA). In addition, increased RKIP expression significantly reduced the phosphorylation of Raf/extracellular signal‐regulated kinase (ERK)/mitogen‐activated protein kinase (MAPK), the transcriptional activity of nuclear factor‐κB (NF‐κB), and the levels of matrix metalloproteinases‐1 and ‐2. In conclusion, these findings clearly demonstrate that RKIP inhibits LX‐2 cell growth, metastasis, and activation, primarily by downregulating the ERK/MAPK and NF‐κB signaling pathways.