scholarly journals Silencing TAK1 alters gene expression signatures in bladder cancer cells

2017 ◽  
Vol 13 (5) ◽  
pp. 2975-2981 ◽  
Author(s):  
Jimin Chen ◽  
Nan Zhang ◽  
Jiaming Wen ◽  
Zhewei Zhang
2020 ◽  
Author(s):  
Shen Pan ◽  
Yunhong Zhan ◽  
Xiaonan Chen ◽  
Bin Wu ◽  
Bitian Liu

Abstract Background T1G3 shows a higher chance of recurrence and progression among early bladder cancer types and the available treatment option is controversial. High recurrence and progression are the problems that need to be explored and solved. Changes in the internal signals of bladder cancer cells and differential genes may be the root cause of these problems. Methods GSE120736, GSE19915, GSE19423, GSE32548 and GSE37815 datasets were obtained from Gene Expression Omnibus (GEO ) to identify differentially expressed genes (DEGs). Bladder cancer transcript data from The Cancer Genome Atlas (TCGA) were clustered into different cell-specific gene sets according to weighted gene co-expression network analysis (WGCNA). Multiple sets of databases were used for gene expression comparison, functional enrichment, and protein interaction analysis, including The Human Protein Atlas, Cancer Dependency Map, Metascape, Gene set enrichment analysis, and DisNor. Results DEGs were obtained through GEO data comparison and intersection. After WGCNA was proven to recognise cell-specific gene sets, candidate DEGs were selected and shown to be specifically expressed in cancer cells. Candidate DEGs were related to mitosis and cell cycle. Further, 12 functional candidate markers were identified from the sequencing data of 30 bladder cancer cell lines. These genes were all up-regulated and previously shown to be closely related to bladder cancer progression. Conclusions Twelve functional genes with specific differential expression in bladder cancer cells were identified. WGCNA can identify the relatively specific expression sets of different cells in bladder cancer with greater tumour heterogeneity, which provides new perspectives for future cancer research.


2016 ◽  
Vol 48 (4) ◽  
pp. 1617-1627 ◽  
Author(s):  
XIAOJUAN XIE ◽  
JINGJING PAN ◽  
LIQIANG WEI ◽  
SHOUZHEN WU ◽  
HUILIAN HOU ◽  
...  

2014 ◽  
Vol 32 (5) ◽  
pp. 2207-2214 ◽  
Author(s):  
SUNG LYEA PARK ◽  
SE YEON WON ◽  
JUN-HUI SONG ◽  
WUN-JAE KIM ◽  
SUNG-KWON MOON

2013 ◽  
Vol 189 (4S) ◽  
Author(s):  
Hyun-Wook Lee ◽  
Hsiang-Tsui Wang ◽  
Mao-wen Weng ◽  
Josephine Kuo ◽  
William C. Huang ◽  
...  

2021 ◽  
Vol 8 ◽  
Author(s):  
Chengle Zhuang ◽  
Changshui Zhuang ◽  
Qun Zhou ◽  
Xueting Huang ◽  
Yaoting Gui ◽  
...  

Aptazyme and CRISPR/Cas gene editing system were widely used for regulating gene expression in various diseases, including cancer. This work aimed to reconstruct CRISPR/Cas13d tool for sensing hTERT exclusively based on the new device OFF-switch hTERT aptazyme that was inserted into the 3’ UTR of the Cas13d. In bladder cancer cells, hTERT ligand bound to aptamer in OFF-switch hTERT aptazyme to inhibit the degradation of Cas13d. Results showed that engineered CRISPR/Cas13d sensing hTERT suppressed cell proliferation, migration, invasion and induced cell apoptosis in bladder cancer 5637 and T24 cells without affecting normal HFF cells. In short, we constructed engineered CRISPR/Cas13d sensing hTERT selectively inhibited the progression of bladder cancer cells significantly. It may serve as a promising specifically effective therapy for bladder cancer cells.


2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Yuchen Liu ◽  
Weiren Huang ◽  
Zhiming Cai

Abstract The logical AND gate gene circuit based on the CRISPR-Cas9 system can distinguish bladder cancer cells from normal bladder epithelial cells. However, the layered artificial gene circuits have the problems of high complexity, difficulty in accurately predicting the behavior, and excessive redundancy, which cannot be applied to clinical translation. Here, we construct minigene circuits based on the CRISPReader, a technology used to control promoter-less gene expression in a robust manner. The minigene circuits significantly induce robust gene expression output in bladder cancer cells, but have nearly undetectable gene expression in normal bladder epithelial cells. The minigene circuits show a higher capability for cancer identification and intervention when compared with traditional gene circuits, and could be used for in vivo cancer gene therapy using the all-in-one AAV vector. This approach expands the design ideas and concepts of gene circuits in medical synthetic biology.


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