Long Non-Coding RNA CASC9 Promotes Bladder Cancer Tumorigenicity and Metastasis via Modulating FZD6/Wnt/β-catenin Signaling Pathway

2020 ◽  
Author(s):  
Yonghao Zhan ◽  
Lianghao Zhang ◽  
Shuanbao Yu ◽  
Xuesong Li ◽  
Yuchen Liu ◽  
...  
Oncotarget ◽  
2017 ◽  
Vol 8 (55) ◽  
pp. 94554-94568 ◽  
Author(s):  
Yangyang Hu ◽  
Chao Deng ◽  
He Zhang ◽  
Jing Zhang ◽  
Bo Peng ◽  
...  

Aging ◽  
2020 ◽  
Vol 12 (16) ◽  
pp. 16021-16034 ◽  
Author(s):  
Hengbing Wang ◽  
Xiaobing Niu ◽  
Hesong Jiang ◽  
Fei Mao ◽  
Bing Zhong ◽  
...  

2020 ◽  
Author(s):  
Hengbing Wang ◽  
Xiaobing Niu ◽  
Hesong Jiang ◽  
Bing Zhong ◽  
Xi Jiang ◽  
...  

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.


2021 ◽  
Author(s):  
Cong Lai ◽  
Zhenyu Wu ◽  
Zhuohang Li ◽  
Hao Yu ◽  
Kuiqing Li ◽  
...  

2020 ◽  
Vol 15 (1) ◽  
pp. 284-295
Author(s):  
Yongtian Zhang ◽  
Dandan Zhao ◽  
Shumei Li ◽  
Meng Xiao ◽  
Hongjing Zhou ◽  
...  

AbstractMultiple myeloma (MM) is a serious health issue in hematological malignancies. Long non-coding RNA taurine-upregulated gene 1 (TUG1) has been reported to be highly expressed in the plasma of MM patients. However, the functions of TUG1 in MM tumorigenesis along with related molecular basis are still undefined. In this study, increased TUG1 and decreased microRNA-34a-5p (miR-34a-5p) levels in MM tissues and cells were measured by the real-time quantitative polymerase reaction assay. The expression of relative proteins was determined by the Western blot assay. TUG1 knockdown suppressed cell viability, induced cell cycle arrest and cell apoptosis in MM cells, as shown by Cell Counting Kit-8 and flow cytometry assays. Bioinformatics analysis, luciferase reporter assay, and RNA pull-down assay indicated that miR-34a-5p was a target of TUG1 and directly bound to notch receptor 1 (NOTCH1), and TUG1 regulated the NOTCH1 expression by targeting miR-34a-5p. The functions of miR-34a-5p were abrogated by TUG1 upregulation. Moreover, TUG1 loss impeded MM xenograft tumor growth in vivo by upregulating miR-34a-5p and downregulating NOTCH1. Furthermore, TUG1 depletion inhibited the expression of Hes-1, Survivin, and Bcl-2 protein in MM cells and xenograft tumors. TUG1 knockdown inhibited MM tumorigenesis by regulating the miR-34a-5p/NOTCH1 signaling pathway in vitro and in vivo, deepening our understanding of the TUG1 function in MM.


Tumor Biology ◽  
2015 ◽  
Vol 36 (10) ◽  
pp. 7685-7689 ◽  
Author(s):  
Li Liu ◽  
Yuchen Liu ◽  
Chengle Zhuang ◽  
Wen Xu ◽  
Xing Fu ◽  
...  

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