scholarly journals Long non-coding RNA CDKN2B antisense RNA 1 gene inhibits Gemcitabine sensitivity in bladder urothelial carcinoma

2018 ◽  
Vol 9 (12) ◽  
pp. 2160-2166 ◽  
Author(s):  
Dalong Xie ◽  
Hui Zhang ◽  
Chao Shang
Keyword(s):  
Urothelial Carcinoma ◽  
Antisense Rna ◽  
Non Coding Rna ◽  
Bladder Urothelial Carcinoma ◽  
Long Non Coding Rna

scholarly journals Long non-coding RNA MEG3 suppresses the development of bladder urothelial carcinoma by regulating miR-96 and TPM1

2018 ◽  
Vol 19 (11) ◽  
pp. 1039-1056 ◽  
Author(s):  
Guanghua Liu ◽  
Xin Zhao ◽  
Jingmin Zhou ◽  
Xiangming Cheng ◽  
Zixing Ye ◽  
...  
Keyword(s):  
Urothelial Carcinoma ◽  
Non Coding Rna ◽  
Bladder Urothelial Carcinoma ◽  
Long Non Coding Rna

scholarly journals Long Non-coding RNA FEZF1-AS1 Promotes Growth and Reduces Apoptosis Through Regulation of miR-363-3p/PAX6 Axis in Retinoblastoma

2021 ◽  
Author(s):  
Xiuming Liu ◽  
Xiaofeng Li ◽  
Jianchang Li
Keyword(s):  
Cell Viability ◽  
Antisense Rna ◽  
Tumor Formation ◽  
Retinoblastoma Cell ◽  
Non Coding Rna ◽  
High Incidence ◽  
Non Coding Rnas ◽  
Long Non Coding Rna ◽  
Common Malignancy

AbstractRetinoblastoma is the most common malignancy in children's eyes with high incidence. Long non-coding RNAs (lncRNAs) play important roles in the progression of retinoblastoma. LncRNA FEZF1 antisense RNA 1 (FEZF1-AS1) has been found to stimulate retinoblastoma. However, the mechanism of FEZF1-AS1 underlying progression of retinoblastoma is still unclear. In current study, FEZF1-AS1 was up-regulated in retinoblastoma tissues and cells. FEZF1-AS1 overexpression enhanced retinoblastoma cell viability, promoted cell cycle, and inhibited apoptosis. Conversely, FEZF1-AS1 knockdown reduced cell viability, cycle, and elevated apoptosis. The interaction between FEZF1-AS1 and microRNA-363-3p (miR-363-3p) was confirmed. FEZF1-AS1 down-regulated miR-363-3p and up-regulated PAX6. PAX6 was a target gene of miR-363-3p. EZF1-AS1 promoted retinoblastoma cell viability and suppressed apoptosis via PAX6. Further, we demonstrated that FEZF1-AS1 contribute to tumor formation in vivo. In conclusion, FEZF1-AS1 elevated growth and inhibited apoptosis by regulating miR-363-3p/PAX6 in retinoblastoma, which provide a new target for retinoblastoma treatment.

Sign in / Sign up

Export Citation Format

Share Document