ZNF655 is involved in development and progression of non-small-cell lung cancer

Non-small cell lung cancer (NSCLC) is a malignant tumor with high mortality, which seriously endangers human health. The clinical significance, biological function and potential mechanism of Zinc finger protein 655 (ZNF655) in NSCLC are discussed in this study. The expression level of ZNF655 in NSCL...

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Bibliographic Details
Published in:Life sciences (1973) 2021-09, Vol.280, p.119727-119727, Article 119727
Main Authors: Teng, Zhihua, Yao, Jie, Zhu, Ling, Zhao, Lufeng, Chen, Gang
Format: Article
Language:English
Subjects:
1-Phosphatidylinositol 3-kinase
AKT protein
Animals
Apoptosis
Bax protein
Carcinoma, Non-Small-Cell Lung - genetics
Carcinoma, Non-Small-Cell Lung - pathology
Caspase-3
Caspase-8
Cell cycle
Cell Line, Tumor
Disease Progression
Female
Gene Expression Regulation, Neoplastic
Humans
Kruppel-Like Transcription Factors - analysis
Kruppel-Like Transcription Factors - genetics
Lung cancer
Lung Neoplasms - genetics
Lung Neoplasms - pathology
Male
Mice
Mice, Inbred BALB C
Middle Aged
Migration
Non-small cell lung carcinoma
NSCLC
p53 Protein
Phosphorylation
Proliferation
Small cell lung carcinoma
Tumorigenesis
Xenografts
Xenotransplantation
Zinc finger proteins
ZNF655
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Summary:Non-small cell lung cancer (NSCLC) is a malignant tumor with high mortality, which seriously endangers human health. The clinical significance, biological function and potential mechanism of Zinc finger protein 655 (ZNF655) in NSCLC are discussed in this study. The expression level of ZNF655 in NSCLC was clarified by immunohistochemical (IHC) staining. Subsequently, lentivirus-mediated shRNA was used to construct ZNF655 knock down NSCLC cells NCI-H1299 and A549. In vitro and in vivo loss of function assays were used to evaluate the malignant behaviors of the cells. The expression level of ZNF655 was abnormally abundant in NSCLC. The decrease of ZNF655 expression led to the inhibition of the malignant behaviors of NSCLC, which was manifested by weakened proliferation, increased sensitivity to apoptosis, cycle repression at G2 and weakened migration. Consistently, downregulation of ZNF655 reduced tumorigenesis in mouse xenograft model. Moreover, decreased expression of ZNF655 resulted in upregulated expression of Bad, Bax, Fas, p21, p27, Caspase 3 and Caspase 8 in NSCLC cells. NCI-H1299 cells with ZNF655 knockdown resulted in decreased phosphorylation of Akt, downregulation of CDK6 and PIK3CA, and upregulation of MAPK9. Collectively, ZNF655 may regulate apoptosis of NSCLC cells through PI3K/Akt and p53 signaling pathways. ZNF655 possessed a promoting effect in the progression of NSCLC, which may serve as a promising molecular target for clinical treatment. [Display omitted]
ISSN:0024-3205
1879-0631
DOI:10.1016/j.lfs.2021.119727