RACK1 expression contributes to JNK activity, but JNK activity does not enhance RACK1 expression in hepatocellular carcinoma SMMC-7721 cells

Receptor for activated C kinase 1 (RACK1) is up-regulated in hepatocellular carcinoma (HCC) and has been reported to augment c-Jun N-terminal protein kinase (JNK) activity in HCC SMMC-7721 cells. By contrast, activator protein-1, a downstream JNK transcription factor, has been revealed to mediate th...

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Bibliographic Details
Published in:Oncology letters 2015-06, Vol.9 (6), p.2767-2770
Main Authors: WANG, WEN-DIE, WEN, ZHI, JI, WENBIN, MA, YUANFANG
Format: Article
Language:English
Subjects:
Apoptosis
c-Jun N-terminal kinases
c-Jun N-terminal protein kinase
Cell culture
Cell growth
Cell receptors
Development and progression
Gene expression
Genetic aspects
Health aspects
Hepatocellular carcinoma
Immunoglobulins
Kinases
Liver cancer
Melanoma
mitogen-activated protein kinase kinase 7
Mutation
Oncology
Phosphorylation
Proteins
Receptor for activated C kinase 1
Studies
Tumorigenesis
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Summary:Receptor for activated C kinase 1 (RACK1) is up-regulated in hepatocellular carcinoma (HCC) and has been reported to augment c-Jun N-terminal protein kinase (JNK) activity in HCC SMMC-7721 cells. By contrast, activator protein-1, a downstream JNK transcription factor, has been revealed to mediate the overexpression of RACK1 in melanoma cells. Therefore, the association between RACK1 and JNK activity in HCC cells has yet to be completely elucidated. The present study analyzed the effects of RACK1 or JNK loss of function on the levels of RACK1 protein, JNK activity, cell proliferation and apoptosis induced by tumor necrosis factor-related apoptosis inducing ligand in HCC SMMC-7721 cells. It was found that JNK loss of function exhibited no effect on RACK1 expression, whereas a loss of RACK1 function led to reduced JNK activity in SMMC-7721 cells. RACK1 and JNK loss of function resulted in the impaired oncogenic growth of SMMC-7721 cells. The present data further support a pivotal role of RACK1 in mediating enhanced JNK activity in HCC cells and also indicate that a novel mechanism exists for RACK1 overexpression in HCC SMMC-7721 cells.
ISSN:1792-1074
1792-1082
DOI:10.3892/ol.2015.3129