CCNY Accelerates Cylcin E Expression to Regulate the Proliferation of Laryngeal Carcinoma Cells via MEK/ERK Signaling Pathway

Xiaoting Zhao,1,2 Mei Jiang,1,2 Ziyu Wang,2 Xiaohong Chen,3 Hongzhen Wang,4 Wentao Yue,1 Chao Cai5,6 1Central Laboratory, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing, People’s Republic of China; 2Department of Cellular and Molecular Biology, Beijing Ches...

Full description

Bibliographic Details
Main Authors: Zhao X, Jiang M, Wang Z, Chen X, Wang H, Yue W, Cai C
Format: Article
Language:English
Published: Dove Medical Press 2020-06-01
Series:Cancer Management and Research
Subjects:
Online Access:https://www.dovepress.com/ccny-accelerates-cylcin-e-expression-to-regulate-the-proliferation-of--peer-reviewed-article-CMAR
_version_ 1818878787857678336
author Zhao X
Jiang M
Wang Z
Chen X
Wang H
Yue W
Cai C
author_facet Zhao X
Jiang M
Wang Z
Chen X
Wang H
Yue W
Cai C
author_sort Zhao X
collection DOAJ
description Xiaoting Zhao,1,2 Mei Jiang,1,2 Ziyu Wang,2 Xiaohong Chen,3 Hongzhen Wang,4 Wentao Yue,1 Chao Cai5,6 1Central Laboratory, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing, People’s Republic of China; 2Department of Cellular and Molecular Biology, Beijing Chest Hospital, Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute, Tongzhou, Beijing, People’s Republic of China; 3Department of Otolaryngology, Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing, People’s Republic of China; 4Department of Oncology, Rizhao City Hospital of Traditional Chinese Medicine, Rizhao, Shandong, People’s Republic of China; 5Beijing YouAn Hospital, Capital Medical University, Beijing, People’s Republic of China; 6Beijing Chest Hospital, Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute, Tongzhou, Beijing, People’s Republic of ChinaCorrespondence: Chao Cai; Wentao Yue Email fangzecai@126.com; yuewt@ccmu.edu.cnBackground: Laryngeal carcinoma is a common cancer among head and neck tumors, accounting for 0.5– 1% new cancer cases or deaths of all tumors throughout the body. Despite improvements in diagnostic and therapy, the prognosis of laryngeal carcinoma patients still remains poor. Thus, it is very important to identify the biomarkers involved in the molecular pathogenesis of laryngeal carcinoma. Cyclin Y (CCNY) is a conserved cell cycle regulator that acts as a growth factor in many cancers. The clinical significance of CCNY in laryngeal carcinoma remains unknown. The function of CCNY in laryngocarcinoma was studied in this paper.Materials and Methods: CCNY knock-out cells were constructed by CRISPR/CAS9 technique. CCNY overexpression cells were also constructed based on CCNY knock-out cells. Cell growth ability was detected by MTS assay, high-content cell analysis, colony formation assays, and anchorage-independent growth assays. The protein levels in laryngocarcinoma cells were determined by Western blot. The role of CCNY in cell cycle progression was evaluated by flow cytometry.Results: CCNY knock-out cells and CCNY up-regulation cell models were obtained successfully. Suppression of CCNY expression inhibited Hep2 cell growth. Cell growth was enhanced by the up-regulation of CCNY. The percentage of cells in G1 phase was altered when CCNY expression was down-regulated or up-regulated. The phosphorylation level of MEK and ERK as well as cyclin E protein level was also regulated by the expression level of CCNY.Conclusion: In laryngocarcinoma cell line Hep2 cells, cell proliferation was controlled by CCNY. The expression of CCNY was involved in the cell cycle progress of Hep2 cells. It indicated that CCNY could promote cell growth by activating MEK/ERK/cyclin E signaling pathway.Keywords: laryngocarcinoma, CCNY, cell cycle, ERK, cyclin E
first_indexed 2024-12-19T14:19:44Z
format Article
id doaj.art-043f856f26564186859189faa100ef41
institution Directory Open Access Journal
issn 1179-1322
language English
last_indexed 2024-12-19T14:19:44Z
publishDate 2020-06-01
publisher Dove Medical Press
record_format Article
series Cancer Management and Research
spelling doaj.art-043f856f26564186859189faa100ef412022-12-21T20:17:49ZengDove Medical PressCancer Management and Research1179-13222020-06-01Volume 124889489854767CCNY Accelerates Cylcin E Expression to Regulate the Proliferation of Laryngeal Carcinoma Cells via MEK/ERK Signaling PathwayZhao XJiang MWang ZChen XWang HYue WCai CXiaoting Zhao,1,2 Mei Jiang,1,2 Ziyu Wang,2 Xiaohong Chen,3 Hongzhen Wang,4 Wentao Yue,1 Chao Cai5,6 1Central Laboratory, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing, People’s Republic of China; 2Department of Cellular and Molecular Biology, Beijing Chest Hospital, Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute, Tongzhou, Beijing, People’s Republic of China; 3Department of Otolaryngology, Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing, People’s Republic of China; 4Department of Oncology, Rizhao City Hospital of Traditional Chinese Medicine, Rizhao, Shandong, People’s Republic of China; 5Beijing YouAn Hospital, Capital Medical University, Beijing, People’s Republic of China; 6Beijing Chest Hospital, Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute, Tongzhou, Beijing, People’s Republic of ChinaCorrespondence: Chao Cai; Wentao Yue Email fangzecai@126.com; yuewt@ccmu.edu.cnBackground: Laryngeal carcinoma is a common cancer among head and neck tumors, accounting for 0.5– 1% new cancer cases or deaths of all tumors throughout the body. Despite improvements in diagnostic and therapy, the prognosis of laryngeal carcinoma patients still remains poor. Thus, it is very important to identify the biomarkers involved in the molecular pathogenesis of laryngeal carcinoma. Cyclin Y (CCNY) is a conserved cell cycle regulator that acts as a growth factor in many cancers. The clinical significance of CCNY in laryngeal carcinoma remains unknown. The function of CCNY in laryngocarcinoma was studied in this paper.Materials and Methods: CCNY knock-out cells were constructed by CRISPR/CAS9 technique. CCNY overexpression cells were also constructed based on CCNY knock-out cells. Cell growth ability was detected by MTS assay, high-content cell analysis, colony formation assays, and anchorage-independent growth assays. The protein levels in laryngocarcinoma cells were determined by Western blot. The role of CCNY in cell cycle progression was evaluated by flow cytometry.Results: CCNY knock-out cells and CCNY up-regulation cell models were obtained successfully. Suppression of CCNY expression inhibited Hep2 cell growth. Cell growth was enhanced by the up-regulation of CCNY. The percentage of cells in G1 phase was altered when CCNY expression was down-regulated or up-regulated. The phosphorylation level of MEK and ERK as well as cyclin E protein level was also regulated by the expression level of CCNY.Conclusion: In laryngocarcinoma cell line Hep2 cells, cell proliferation was controlled by CCNY. The expression of CCNY was involved in the cell cycle progress of Hep2 cells. It indicated that CCNY could promote cell growth by activating MEK/ERK/cyclin E signaling pathway.Keywords: laryngocarcinoma, CCNY, cell cycle, ERK, cyclin Ehttps://www.dovepress.com/ccny-accelerates-cylcin-e-expression-to-regulate-the-proliferation-of--peer-reviewed-article-CMARlaryngocarcinomaccnycell cycleerkcyclin e
spellingShingle Zhao X
Jiang M
Wang Z
Chen X
Wang H
Yue W
Cai C
CCNY Accelerates Cylcin E Expression to Regulate the Proliferation of Laryngeal Carcinoma Cells via MEK/ERK Signaling Pathway
Cancer Management and Research
laryngocarcinoma
ccny
cell cycle
erk
cyclin e
title CCNY Accelerates Cylcin E Expression to Regulate the Proliferation of Laryngeal Carcinoma Cells via MEK/ERK Signaling Pathway
title_full CCNY Accelerates Cylcin E Expression to Regulate the Proliferation of Laryngeal Carcinoma Cells via MEK/ERK Signaling Pathway
title_fullStr CCNY Accelerates Cylcin E Expression to Regulate the Proliferation of Laryngeal Carcinoma Cells via MEK/ERK Signaling Pathway
title_full_unstemmed CCNY Accelerates Cylcin E Expression to Regulate the Proliferation of Laryngeal Carcinoma Cells via MEK/ERK Signaling Pathway
title_short CCNY Accelerates Cylcin E Expression to Regulate the Proliferation of Laryngeal Carcinoma Cells via MEK/ERK Signaling Pathway
title_sort ccny accelerates cylcin e expression to regulate the proliferation of laryngeal carcinoma cells via mek erk signaling pathway
topic laryngocarcinoma
ccny
cell cycle
erk
cyclin e
url https://www.dovepress.com/ccny-accelerates-cylcin-e-expression-to-regulate-the-proliferation-of--peer-reviewed-article-CMAR
work_keys_str_mv AT zhaox ccnyacceleratescylcineexpressiontoregulatetheproliferationoflaryngealcarcinomacellsviamekerksignalingpathway
AT jiangm ccnyacceleratescylcineexpressiontoregulatetheproliferationoflaryngealcarcinomacellsviamekerksignalingpathway
AT wangz ccnyacceleratescylcineexpressiontoregulatetheproliferationoflaryngealcarcinomacellsviamekerksignalingpathway
AT chenx ccnyacceleratescylcineexpressiontoregulatetheproliferationoflaryngealcarcinomacellsviamekerksignalingpathway
AT wangh ccnyacceleratescylcineexpressiontoregulatetheproliferationoflaryngealcarcinomacellsviamekerksignalingpathway
AT yuew ccnyacceleratescylcineexpressiontoregulatetheproliferationoflaryngealcarcinomacellsviamekerksignalingpathway
AT caic ccnyacceleratescylcineexpressiontoregulatetheproliferationoflaryngealcarcinomacellsviamekerksignalingpathway