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ONCOLOGY / CLINICAL RESEARCH
ERK knockdown suppresses cell biological activities via regulation of CD59 in breast cancer
1
Jiangxi University of Traditional Chinese Medicine, Nanchang, China
2
Department of Breast Surgery, The Third Hospital of Nanchang, Jiangxi, China
3
Jiangxi Province Key Laboratory for Breast Diseases Nanchang, Jiangxi, China
Submission date: 2021-05-24
Final revision date: 2021-06-10
Acceptance date: 2021-07-02
Online publication date: 2021-08-07
Corresponding author
KEYWORDS
TOPICS
ABSTRACT
Introduction:
The purpose of this study was to investigate the effect of extracellular signal-regulated kinase (ERK) in breast cancer and the related mechanisms.
Material and methods:
Some previous studies found that ERK was closely correlated with CD59 in cancer. In our clinical study, we evaluated ERK and CD59 protein expression in different tissue from patients by immunohistochemical (IHC) assay using MCF-7 and MDA-MB-231 cell lines which were breast cancer cell lines as target cell lines. We performed an in vitro study, evaluating cell biological activities including proliferation, apoptosis, cell cycle, invasion, adherent and migration by MTT, clone test, TUNEL assay, flow cytometry and wound healing, and measuring relative protein expression by WB assay. In an in vivo study, measuring tumor weight and volume, the apoptosis cell number was evaluated by TUNEL assay and relative protein expression by IHC assay.
Results:
Compared with adjacent normal tissue, the ERK and CD59 protein expression levels were significantly increased in breast cancer tissues (both p < 0.001). In in vitro and in vivo studies, with ERK knockdown, the cell biological activities were significantly depressed with CD59 suppression (both p < 0.001). Also the relative protein levels including CD59, PKD, P53, E-cadherin and vimentin were significantly different (each p < 0.001).
Conclusions:
ERK act as an oncology gene in breast cancer development. ERK inhibitor suppressed breast cancer biologically via regulation of CD59 in vitro and in vivo.
The purpose of this study was to investigate the effect of extracellular signal-regulated kinase (ERK) in breast cancer and the related mechanisms.
Material and methods:
Some previous studies found that ERK was closely correlated with CD59 in cancer. In our clinical study, we evaluated ERK and CD59 protein expression in different tissue from patients by immunohistochemical (IHC) assay using MCF-7 and MDA-MB-231 cell lines which were breast cancer cell lines as target cell lines. We performed an in vitro study, evaluating cell biological activities including proliferation, apoptosis, cell cycle, invasion, adherent and migration by MTT, clone test, TUNEL assay, flow cytometry and wound healing, and measuring relative protein expression by WB assay. In an in vivo study, measuring tumor weight and volume, the apoptosis cell number was evaluated by TUNEL assay and relative protein expression by IHC assay.
Results:
Compared with adjacent normal tissue, the ERK and CD59 protein expression levels were significantly increased in breast cancer tissues (both p < 0.001). In in vitro and in vivo studies, with ERK knockdown, the cell biological activities were significantly depressed with CD59 suppression (both p < 0.001). Also the relative protein levels including CD59, PKD, P53, E-cadherin and vimentin were significantly different (each p < 0.001).
Conclusions:
ERK act as an oncology gene in breast cancer development. ERK inhibitor suppressed breast cancer biologically via regulation of CD59 in vitro and in vivo.
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| eISSN: | 1896-9151 |
| ISSN: | 1734-1922 |
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