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Carboxy-terminus Hsc70 interacting protein exerts a tumor inhibition function in head and neck cancer
Author(s) -
Xiao Meng,
Ming Yan,
Jianjun Zhang,
Qin Xu,
Wantao Chen
Publication year - 2017
Publication title -
oncology reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.094
H-Index - 96
eISSN - 1791-2431
pISSN - 1021-335X
DOI - 10.3892/or.2017.5827
Subject(s) - oncogene , in vivo , gene knockdown , tissue microarray , ubiquitin , cancer research , ubiquitin ligase , biology , cancer , molecular medicine , microbiology and biotechnology , chemistry , apoptosis , cell cycle , biochemistry , gene , genetics
Several independent studies have reported the roles of the E3 ubiquitin ligase, carboxy-terminus Hsc70 interacting protein (CHIP) in various types of cancers. However, the biological effects of CHIP vary in regards to different cancers, and the role of CHIP in head and neck cancers (HNCs) remains unknown. In the present study, CHIP overexpression plasmids and CHIP knockdown lentivirus were constructed to affect the expression levels of CHIP protein and biological behaviors in HNC cell lines bilaterally. The biological behaviors regulated by CHIP in HNCs were investigated both in vivo and in vitro with a series of assays and analyses. A tissue microarray was stained and analyzed for the clinical significance of CHIP expression in HNCs. We identified that CHIP suppressed the malignant behaviors of HNCs in a series of in vitro and in vivo experiments, but not its two loss-of-function mutants. However, we observed an altered expression pattern of CHIP from a well, moderate, to poor differentiation pathological status in HNC specimens. In a retrospective cohort of HNCs, lower expression of CHIP indicated a poor differentiation status in tumors and a lower overall survival rate. The present study demonstrated that CHIP functions as a tumor suppressor in HNCs. In conclusion, we demonstrated that suppressed expression of CHIP may result in the progression of HNCs.

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