lncRNA CCAT1 promotes bladder cancer cell proliferation, migration and invasion

Zhang, Caixiang; Wang, Wenying; Lin, Jun; Xiao, Jing; Tian, Ye

doi:10.1590/s1677-5538.ibju.2018.0450

Cited by 64 publications

(43 citation statements)

References 28 publications

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“…However, there are still no effective therapies for NSCLC treatment in clinic [2], uncovering the underlying mechanisms of NSCLC pathogenesis might solve this problem. Long-noncoding RNAs (lncRNAs) was closely related with the development of multiple cancers, such as bladder cancer [3], gastric cancer [4], ovarian cancer [5] and NSCLC [6]. For example, lncRNA LINC-PINT inhibited NSCLC progression by targeting miR-218-5p/PDCD4 [6] and LncRNA AWPPH promoted NSCLC cell proliferation by activating Wnt/β-catenin signaling pathway [7].…”

Section: Introductionmentioning

confidence: 99%

Downregulation of LncRNA-XIST inhibited development of non-small cell lung cancer by activating miR-335/SOD2/ROS signal pathway mediated pyroptotic cell death

Liu

Yao

Zhang

et al. 2019

Aging

165

130

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LncRNA-XIST participated in the regulation of Non-small cell lung cancer (NSCLC) progression, but the underlying mechanisms are still unclear. This study showed that LncRNA-XIST aberrantly overexpressed in either NSCLC tissues or cell lines comparing to their paired control groups. Knock-down of LncRNA-XIST promoted NSCLC cell apoptosis and inhibited cell proliferation, which were reversed by synergistically treating cells with pyroptosis inhibitor Necrosulfonamide (NSA). In addition, knock-down of LncRNA-XIST also promoted reactive oxygen species (ROS) production and NLRP3 inflammasome activation. In parallel, ROS scavenger N-acetyl cysteine (NAC) abrogated the effects of downregulated LncRNA-XIST on NSCLC cell pyroptosis. Furthermore, miR-335 was the downstream target of LncRNA-XIST and overexpressed LncRNA-XIST increased SOD2 expression levels by sponging miR-335. Mechanistically, miR-335 inhibitor reversed the effects of downregulated LncRNA-XIST on ROS levels and cell pyroptosis, which were abrogated by synergistically knocking down SOD2. Taken together, knock-down of LncRNA-XIST inhibited NSCLC progression by triggering miR-335/SOD2/ROS signal pathway mediated pyroptotic cell death.

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Section: Introductionmentioning

confidence: 99%

Downregulation of LncRNA-XIST inhibited development of non-small cell lung cancer by activating miR-335/SOD2/ROS signal pathway mediated pyroptotic cell death

Liu

Yao

Zhang

et al. 2019

Aging

165

130

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“…GAS5 overexpression significantly decreased viability and increased apoptosis of BC cells [13]. Abnormal expression of CCAT1 facilitates cell proliferation, invasion, and migration in BC [14]. Moreover, CASC9 has been identified as a tumor promoter in multiple cancers.…”

Section: Introductionmentioning

confidence: 99%

CASC9 Facilitates Cell Proliferation in Bladder Cancer by Regulating CBX2 Expression

Huo

Tan

Chen

2020

Nephron

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Background: As the seventh most common urologic carcinoma worldwide, approximately 430,000 patients are diagnosed with bladder cancer (BC) every year. Increasing evidence indicates that long noncoding RNAs (lncRNAs) play crucial roles in the progression of BC. Objectives: This study is aimed to explore the function and mechanism of CASC9 in BC. Methods: Bioinformatics analysis and experiments including RT-qPCR, luciferase reporter, Cell Counting Kit-8 assay, Western blot, RNA immunoprecipitation assay, and TU-NEL staining were applied to explore the function and mechanism of CASC9 in BC tissues and cell lines. Results: Our study demonstrated that CASC9 was upregulated in BC tissues and cell lines. Moreover, we found that CASC9 knockdown notably decreased proliferation while increased apoptotic rate in BC cells. Mechanistically, bioinformatics prediction and following experiments indicated that CASC9 worked as a competing endogenous RNA (ceRNA) of CBX2 through sponging miR-497-5p. Meanwhile, we recognized that CASC9 and miR-497-5p negatively regulated each other in a mutual way. Furthermore, we found that miR-497-5p shared binding site with CBX2. In addition, miR-497-5p could negatively regulated CBX2, while CASC9 could positively regulated CBX2. Rescue assays reveled that CBX2 overexpression could reversed the reduction of cell proliferation or the enhancement of cell apoptosis induced by CASC9 suppression. Conclusions: Our study manifests the first evidence that CASC9 serves as an oncogene in BC and accelerates cell proliferation by modulating miR-497-5p/CBX2 axis. The present study may provide a cogitable target for BC therapy.

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“…MYC is an oncogene involved in cell cycle regulation, cell adhesion, cell growth arrest, metabolism, protein synthesis, ribosome biogenesis and mitochondrial function, which has been described as a crucial element of numerous human carcinogenesis processes, such as GC [31][32][33][34]. MiRanda database showed binding sites of miR-145 and miR-1304 in the 3 0 noncoding region of MYC.…”

Section: Discussionmentioning

confidence: 99%

Circ-PRMT5 promotes gastric cancer progression by sponging miR-145 and miR-1304 to upregulate MYC

Wei

Ding

Guo

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Background: Gastric cancer (GC) is a global leading source of cancer-associated deaths. Circular RNAs (circRNAs) are a new type of non-coding RNA and promising biomarkers for diagnosis of multiple diseases such as cancer. Methods: Circ-PRMT5 expression was validated in 90 GC patient tissues and 6 different GC cells by qRT-PCR. Sublocalization of circ-PRMT5 in GC cells was determined in isolated nuclear and cytoplasmic RNAs. CircInteractome and miRanda were used to predict binding sites between circ-PRMT5 with micRNAs, and micRNAs with target mRNA. The correlation between genes was determined by the Pearson correlation analysis. The molecular mechanism was demonstrated by RNA in vivo precipitation, point mutation, luciferase activity and rescue experiments. Results: Circ-PRMT5 expression was significantly higher in GC than in adjacent normal tissues, and GC patients with circ-PRMT5 high expression had shorter survival times. Functionally, circ-PRMT5 silence inhibited GC cell growth and invasion. Mechanism analysis showed that circ-PRMT5 sponged miR-145/ miR-1304 to upregulate MYC expression and GC development. Conclusion: Our findings demonstrated that circ-PRMT5 function as an oncogene in GC patients by targeting miR-145/miR-1304/MYC axis. High circ-PRMT5 expression may provide a poor prognostic indicator of survival in GC patients and targeting circ-PRMT5/miR-145/miR-1304/MYC axis may be a novel therapeutic strategy for GC.

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lncRNA CCAT1 promotes bladder cancer cell proliferation, migration and invasion

Cited by 64 publications

References 28 publications

Downregulation of LncRNA-XIST inhibited development of non-small cell lung cancer by activating miR-335/SOD2/ROS signal pathway mediated pyroptotic cell death

Downregulation of LncRNA-XIST inhibited development of non-small cell lung cancer by activating miR-335/SOD2/ROS signal pathway mediated pyroptotic cell death

CASC9 Facilitates Cell Proliferation in Bladder Cancer by Regulating CBX2 Expression

Circ-PRMT5 promotes gastric cancer progression by sponging miR-145 and miR-1304 to upregulate MYC

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