scholarly journals Long non-coding RNA DLX6-AS1 facilitates bladder cancer progression through modulating miR-195-5p/VEGFA signaling pathway

Aging ◽  
2020 ◽  
Vol 12 (16) ◽  
pp. 16021-16034 ◽  
Author(s):  
Hengbing Wang ◽  
Xiaobing Niu ◽  
Hesong Jiang ◽  
Fei Mao ◽  
Bing Zhong ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Long non-coding RNA LINC00662 facilitates bladder cancer progression through modulating miR-195-5p/VEGFA/Ras/Raf/MEK/ERK signaling pathway

2020 ◽  
Author(s):  
Hengbing Wang ◽  
Xiaobing Niu ◽  
Hesong Jiang ◽  
Bing Zhong ◽  
Xi Jiang ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Malignant Tumors ◽  
Erk Signaling ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Non Coding Rna ◽  
Gene Assay ◽  
Long Non Coding Rna

Abstract Background: Bladder cancer (BC) is one of the most common malignant tumors in the urinary system. Long non-coding RNA (lncRNA) plays an important role in BC. Methods: LINC00662 expression was identified by quantitative real-time polymerase chain reaction (qPCR) and in situ hybridization (ISH). The effect of LINC00662 on cell proliferation, apoptosis, migration and invasion was measured by CCK8 assay, colony formation assay, transwell assay, and western blot. Dual-luciferase reporter gene assay, RNA pull-down and RIP assay confirm the interaction between LINC00662 and miR-195-5p/VEGFA. The in vivo effect of LINC00662 on BC was investigated using a mouse tumorigenicity model. Results: LINC00662 was overexpressed in BC tissues and cell lines, and negatively correlated with the survival of BC patients. Overexpression of LINC00662 promoted proliferation, migration and invasion and inhibited apoptosis of BC cells, and LINC00662 knockdown abrogated this effect. Silencing LINC00662 inhibited BC growth in a subcutaneous BC tumor mouse model. LINC00662 acted as an oncogene through regulating miR-195-5p/VEGFA axes. Decreased VEGFA expression caused by LINC00662 knockdown inhibited the phosphorylation of Raf-1, MEK1/2, and ERK1/2, while this regulation effect was abrogated by miR-195-5p inhibitor. Conclusion: LINC00662 regulated the proliferation, apoptosis, migration, and invasion of BC cells probably via miR-195-5p-mediated VEGFA/Ras/Raf/MEK/ERK signaling pathway.

scholarly journals Long non-coding RNA XIST promotes cell growth and metastasis through regulating miR-139-5p mediated Wnt/β-catenin signaling pathway in bladder cancer

Oncotarget ◽  
2017 ◽  
Vol 8 (55) ◽  
pp. 94554-94568 ◽  
Author(s):  
Yangyang Hu ◽  
Chao Deng ◽  
He Zhang ◽  
Jing Zhang ◽  
Bo Peng ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Growth ◽  
Signaling Pathway ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Knockdown of Long Non-coding RNA SNGH3 by CRISPR-dCas9 Inhibits the Progression of Bladder Cancer

2021 ◽  
Vol 8 ◽  
Author(s):  
Yu Cao ◽  
Qiong Hu ◽  
Ruiming Zhang ◽  
Ling Li ◽  
Mingjuan Guo ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Progression ◽  
Research Evidence ◽  
Histological Grade ◽  
Non Coding Rna ◽  
Clinical Relationship ◽  
Non Coding Rnas ◽  
Cancer Tissues ◽  
Long Non Coding Rna ◽  
Nucleolar Rna

Recent research evidence documents that lncRNAs (long non-coding RNAs lncRNAs) play a pivotal role in the tumorigenesis and development of tumors. LncRNA SNGH3 (small nucleolar RNA host gene 3) is highly expressed in numerous forms of cancer, serving as an oncogene in cancer progression. Nonetheless, the clinical relationship, along with the mechanism of SNGH3 in bladder cancer, have not been studied. Herein, the findings exhibited upregulation of SNGH3 in bladder cancer tissues, along with the cell lines. Furthermore, overexpressed SNGH3 was positively linked to the TNM stage, as well as the histological grade of bladder cancer. Moreover, the silencing of SNGH3, using CRISPR-dCas9, suppressed cell growth along with migration, but elevated bladder cancer cell apoptosis. In summary, we established that SNGH3 serves as a bladder cancer oncogene and could be employed as a prospective diagnostic marker for clinical use, and is also a therapeutic target for CRISPR-mediated gene therapy.

Sign in / Sign up

Export Citation Format

Share Document