scholarly journals High Expression of KIF22/Kinesin-Like DNA Binding Protein (Kid) as a Poor Prognostic Factor in Prostate Cancer Patients

2018 ◽  
Vol 24 ◽  
pp. 8190-8197 ◽  
Author(s):  
Zheng Zhang ◽  
Hui Xie ◽  
Shimiao Zhu ◽  
Xuanrong Chen ◽  
Jianpeng Yu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Prognostic Factor ◽  
Dna Binding ◽  
Cancer Patients ◽  
Binding Protein ◽  
Dna Binding Protein ◽  
High Expression ◽  
Poor Prognostic Factor

scholarly journals Role of Damage DNA-Binding Protein 1 in Pancreatic Cancer Progression and Chemoresistance

Cancers ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 1998 ◽  
Author(s):  
Yiyin Zhang ◽  
Yubin Lei ◽  
Jin Xu ◽  
Jie Hua ◽  
Bo Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Dna Binding ◽  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
Binding Protein ◽  
Dna Binding Protein ◽  
High Expression ◽  
Pdac Cell ◽  
Mesenchymal Transition ◽  
Damaged Dna

Damaged DNA-binding protein 1 (DDB1) recruits nucleotide excision pathway proteins to form the UV-damaged DNA-binding protein complex and is required for DNA repair. DDB1 was reported to participate in apoptosis and chemoresistance regulation in several cancers. However, little is known about the function of DDB1 in pancreatic adenocarcinoma (PDAC). In this study, we reported that DDB1 functions as a tumor-promoting factor in PDAC by regulating cancer cell proliferation, epithelial-mesenchymal transition (EMT) and chemoresistance. Compared to normal pancreatic tissues, PDAC tissues had high expression levels of DDB1, and this high expression was positively correlated with poor prognosis. Furthermore, reductions in cell proliferation and EMT were observed in DDB1-deficient PDAC cell lines. Intriguingly, we also found that abrogation of DDB1 expression increased PDAC cell sensitivity to gemcitabine (GEM). Mechanistically, DDB1 knockdown was associated with an increase in deoxycytidine kinase expression in vivo and in vitro. In summary, our work demonstrated that DDB1 promotes PDAC progression and chemoresistance and may serve as a potential predictive marker and therapeutic target for PDAC treatment.

scholarly journals The role of chromodomain helicase DNA binding protein 1 (CHD1) in promoting an invasive prostate cancer phenotype

2021 ◽  
Vol 13 ◽  
pp. 175628722110224
Author(s):  
Aparna Kareddula ◽  
Daniel J. Medina ◽  
Whitney Petrosky ◽  
Sonia Dolfi ◽  
Irina Tereshchenko ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Dna Binding ◽  
Adhesion Molecules ◽  
Binding Protein ◽  
Dna Binding Protein ◽  
Matrix Metalloproteinase 2 ◽  
Epithelial Cell Line ◽  
Target Cells ◽  
Integrin Subunit ◽  
Suspension Cells

Background: Prostate cancer (PCa) phenotypes vary from indolent to aggressive. Molecular subtyping may be useful in predicting aggressive cancers and directing therapy. One such subtype involving deletions of chromodomain helicase DNA binding protein 1 ( CHD1), a tumor suppressor gene, are found in 10–26% of PCa tumors. In this study, we evaluate the functional cellular effects that follow CHD1 deletion. Methods: CHD1 was knocked out (KO) in the non-tumorigenic, human papillomavirus 16 (HPV16)-immortalized prostate epithelial cell line, RWPE-1, using CRISPR/Cas9. In vitro assays such as T7 endonuclease assay, western blot, and sequencing were undertaken to characterize the CHD1 KO clones. Morphologic and functional assays for cell adhesion and viability were performed. To study expression of extracellular matrix (ECM) and adhesion molecules, a real-time (RT) profiler assay was performed using RWPE-1 parental, non-target cells (NT2) and CHD1 KO cells. Result: Compared to parental RWPE-1 and non-target cells (NT2), the CHD1 KO cells had a smaller, rounder morphology and were less adherent under routine culture conditions. Compared to parental cells, CHD1 KO cells showed a reduction in ECM and adhesion molecules as well as a greater proportion of viable suspension cells when cultured on standard tissue culture plates and on plates coated with laminin, fibronectin or collagen I. CHD1 KO cells showed a decrease in the expression of secreted protein acidic and rich in cysteine (SPARC), matrix metalloproteinase 2 (MMP2), integrin subunit alpha 2 (ITGA2), integrin subunit alpha 5 (ITGA5), integrin subunit alpha 6 (ITGA6), fibronectin (FN1), laminin subunit beta-3 precursor (LAMB3), collagen, tenascin and vitronectin as compared to parental and NT2 cells. Conclusion: These data suggest that in erythroblast transformation specific (ETS) fusion-negative, phosphatase and tensin homolog ( PTEN) wildtype PCa, deletion of CHD1 alters cell-cell and cell-matrix adhesion dynamics, suggesting an important role for CHD1 in the development and progression of PCa.

scholarly journals Frequent Disruption of Chromodomain Helicase DNA-Binding Protein 8 (CHD8) and Functionally Associated Chromatin Regulators in Prostate Cancer

Neoplasia ◽  
2014 ◽  
Vol 16 (12) ◽  
pp. 1018-1027 ◽  
Author(s):  
Nathan A. Damaschke ◽  
Bing Yang ◽  
Michael L. Blute ◽  
Chee Paul Lin ◽  
Wei Huang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Dna Binding ◽  
Binding Protein ◽  
Dna Binding Protein ◽  
Chromatin Regulators

The DNA-binding protein YB-1 is a direct MYCN target and influences repair and resistance in neuroblastoma cell lines

2010 ◽  
Vol 222 (03) ◽  
Author(s):  
S Degen ◽  
S Kuhfittig-Kulle ◽  
JH Schulte ◽  
F Westermann ◽  
A Schramm ◽  
...  
Keyword(s):  
Dna Binding ◽  
Cell Lines ◽  
Binding Protein ◽  
Neuroblastoma Cell ◽  
Dna Binding Protein ◽  
Neuroblastoma Cell Lines
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