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

Teng, Zhihua; Yao, Jie; Zhu, Ling; Zhao, Lufeng; Chen, Gang

doi:10.1016/j.lfs.2021.119727

Cited by 7 publications

(8 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, a previous study clarified that ZNF655 was downregulated in glioma-associated endothelial cells, whose overexpression could inhibit the angiogenesis of glioma-associated endothelial cells ( 19 ). Moreover, ZNF655 possessed a promoting effect in the progression of non-small cell lung cancer ( 20 ). However, the biological functions and underlying molecular mechanisms of ZNF655 in glioma cells are still unknown.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: ZNF655 Promotes the Progression of Glioma Through Transcriptional Regulation of AURKA

et al. 2022

View full text Add to dashboard Cite

ObjectivesGlioma has a high degree of malignancy, strong invasiveness, and poor prognosis, which is always a serious threat to human health. Previous studies have reported that C2H2 zinc finger (ZNF) protein is involved in the progression of various cancers. In this study, the clinical significance, biological behavior, and molecule mechanism of ZNF655 in glioma were explored.MethodsThe expression of ZNF655 in glioma and its correlation with prognosis were analyzed through public datasets and immunohistochemical (IHC) staining. The shRNA-mediated ZNF655 knockdown was used to explore the effects of ZNF655 alteration on the phenotypes and tumorigenesis of human glioma cell lines. Chromatin immunoprecipitation (ChIP)-qPCR and luciferase reporter assays were performed to determine the potential mechanism of ZNF655 regulating Aurora kinase A (AURKA).ResultsZNF655 was abundantly expressed in glioma tissue and cell lines SHG-44 and U251. Knockdown of suppressed the progression of glioma cells, which was characterized by reduced proliferation, enhanced apoptosis, cycle repression in G2, inhibition of migration, and weakened tumorigenesis. Mechanistically, transcription factor ZNF655 activated the expression of AURKA by directly binding to the promoter of AURKA. In addition, downregulation of AURKA partially reversed the promoting effects of overexpression of ZNF655 on glioma cells.ConclusionsZNF655 promoted the progression of glioma by binding to the promoter of AURKA, which may be a promising target for molecular therapy.

show abstract

Section: Introductionmentioning

confidence: 99%

RETRACTED: ZNF655 Promotes the Progression of Glioma Through Transcriptional Regulation of AURKA

et al. 2022

View full text Add to dashboard Cite

show abstract

“…For example, Chen et al, indicated that ZNF655 promotes the progression of glioma through transcriptional regulation of AURKA [33]. Teng et al, demonstrated that the decrease of ZNF655 expression led to the inhibition of the malignant behaviors of nonsmall cell lung cancer, which was manifested by weakened proliferation, increased sensitivity to apoptosis, cycle repression at G2 and weakened migration [34]. Yang et al, identified role of ANKHD1/LINC00346/ZNF655 feedback loop in regulating the glioma angiogenesis via staufen1-mediated mRNA decay [35].…”

Section: Discussionmentioning

confidence: 99%

ZNF655 accelerates progression of pancreatic cancer by promoting the binding of E2F1 and CDK1

Shao

Qiao

et al. 2022

Oncogenesis

View full text Add to dashboard Cite

Pancreatic cancer has an extremely terrible prognosis and is a common cause of cancer death. In this study, the clinic value, biological function and underlying mechanisms of Zinc finger protein 655 (ZNF655) in human pancreatic cancer were evaluated. The expression level of ZNF655 in pancreatic cancer was determined by immunohistochemistry (IHC) staining. The biological effects of ZNF655 in pancreatic cancer cells was investigated by loss/gain-of-function assays in vitro and in vivo. The downstream molecular mechanism of ZNF655 was explored using co-immunoprecipitation (Co-IP), dual-luciferase reporter and chromatin immunoprecipitation (Ch-IP). ZNF655 expression was significantly elevated in human pancreatic cancer and possessed clinical value in predicting poor prognosis. Functionally, ZNF655 knockdown inhibited the biological progression of pancreatic cancer cells, which was characterized by weaken proliferation, enhanced apoptosis, arrested cell cycle in G2, impeded migration, and suppressed tumor growth. Mechanistically, ZNF655 played an important role in promoting the binding of E2F transcription factor 1 (E2F1) to the cyclin-dependent kinase 1 (CDK1) promoter. Furthermore, knockdown of CDK1 alleviated the promoting effects of ZNF655 overexpression in pancreatic cancer cells. The promotive role of ZNF655 in pancreatic cancer via CDK1 was determined, which drew further interest regarding its clinical application as a promising therapeutic target.

show abstract

“…MAPK9 is most closely related to MAPK8, and both are known as C-Jun N-terminal kinase, which can block tumor suppressor p53 ( Topisirovic et al, 2009 ; Barutcu and Girnius 2018 ). MAPK9 signaling pathway is reported to have regulatory roles in non-small cell lung cancer, bladder cancer, cholangiocarcinoma and other cancers ( Hao et al, 2021 ; Huang et al, 2021 ; Teng et al, 2021 ). Meanwhile, it also has a great potential as the biomarker ( Song et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

Screening of ferroptosis-related genes with prognostic effect in colorectal cancer by bioinformatic analysis

Zhou

Wang

et al. 2022

Front. Mol. Biosci.

View full text Add to dashboard Cite

Colorectal cancer (CRC) remains a common malignant tumor of digestive tract with high incidence rate and high mortality in the worldwide. The current clinical treatments of CRC often fail to achieve satisfactory results. Searching for more effective prediction or prognosis biomarkers, or developing more targeted therapeutic schedule may help to improve the outcomes of CRC patients. Here, we tried to study the effect of ferroptosis-related genes on CRC prognosis and make it clearer that ferroptosis has connection with immune environment. First, we obtained gene expression data of CRC and normal tissues, as well as corresponding clinical data from the Gene Expression Omnibus (GEO) database and the Cancer Genome Atlas (TCGA) database. The differentially expressed genes (DEGs) were intersected with ferroptosis-related gene set downloaded from FerrDb database, and 93 abnormally expressed ferroptosis-related genes were obtained. Then, these genes were analyzed for functional enrichment. Univariate Cox regression and multivariate Cox regression analyses were performed to establish prognostic model based on ferroptosis-related genes. In the process of exploring the correlation between prognostic genes and immune infiltration, we found that these genes were closely related to B cells, CD8+ T cells, CD4+ T cells, macrophages and other cells in CRC. In addition, we found a large proportion of plasma cells and macrophages in TCGA-COADREAD. Finally, a prognostic nomogram of ferroptosis-related genes was established, including age, sex, grade and other predicted values. To summary, we established a prognostic model of colorectal cancer (CRC) based on ferroptosis-related genes and further explored the relationship between these genes with immune microenvironment.

show abstract

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

Cited by 7 publications

References 28 publications

RETRACTED: ZNF655 Promotes the Progression of Glioma Through Transcriptional Regulation of AURKA

RETRACTED: ZNF655 Promotes the Progression of Glioma Through Transcriptional Regulation of AURKA

ZNF655 accelerates progression of pancreatic cancer by promoting the binding of E2F1 and CDK1

Screening of ferroptosis-related genes with prognostic effect in colorectal cancer by bioinformatic analysis

Contact Info

Product

Resources

About