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Knockdown of CHPF suppresses cell progression of non-small-cell lung cancer

Authors Hou XM, Baloch Z, Zheng ZH, Zhang WH, Feng Y, Li DD, Wu XA, Yang SH

Received 24 October 2018

Accepted for publication 7 March 2019

Published 24 April 2019 Volume 2019:11 Pages 3275—3283

DOI https://doi.org/10.2147/CMAR.S192036

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Andrew Yee

Peer reviewer comments 2

Editor who approved publication: Dr Rituraj Purohit


Xiao-Ming Hou,1,2 Zulqarnain Baloch,3,4 Zhan-Hong Zheng,3,4 Wen-Hui Zhang,1,2 Ying Feng,5 Duan-Duan Li,3,4 Xin-An Wu,2,6 Shi-Hua Yang3,4

1Department of Oncology, The First Hospital of Lanzhou University, Lanzhou 730000, People’s Republic of China; 2Key Laboratory of Biotherapy and Regenerative Medicine of Gansu Province, The First Hospital of Lanzhou University, Lanzhou 730000, People’s Republic of China; 3College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, People’s Republic of China; 4Key Laboratory of Comprehensive Prevention and Control for Severe Clinical Animal Diseases of Guangdong Province, South China Agricultural University, Guangzhou 510642, People’s Republic of China; 5Department of Pathology, The First Hospital of Lanzhou University, Lanzhou 730000, People’s Republic of China; 6Department of Pharmacy, The First Hospital of Lanzhou University, Lanzhou 730000, People’s Republic of China

Purpose: The aim of the present study was to explore the role of CHPF in non-small-cell lung cancer (NSCLC) and to develop an shRNA vector-based therapy to repress the expression of CHPF gene in NSCLC cell lines.
Methods: In this study, we used immunohistochemical staining to verify the expression of CHPF in NSCLC tissue. Then, we determined the expression of CHPF gene in different NSCLC cell lines with RT-PCR and Western blotting. Specific CHPF shRNA was used to knockdown the expression of CHPF. Celigo image cytometry, cell cycle analysis, and flow cytometry assay were performed.
Results: The results showed that expression level of CHPF was higher in NSCLC tissues than normal lung tissues. Further, we established that CHPF expression knockdown in NSCLC cells could substantially restrain the cell proliferation, apoptosis, and cell cycle in vitro.
Conclusion: On the basis of these results, we concluded that CHPF expression has an important role in the progression of human NSCLC cells. Therefore, its interference could possibly be used as a potential therapeutic target against NSCLC.

Keywords: NSCLC, CHPF, progression, knockdown

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