Knockdown of Long Noncoding RNA CCAT2 Inhibits Cellular Proliferation, Invasion, and Epithelial‐Mesenchymal Transition in Glioma Cells

Zeng, Jing; Du, Tianping; Song, Yafeng; Gao, Yan; Li, Fuyan; Wu, Ruimin; Chen, Yijia; Li, Wei; Zhou, Hong; Yang, Yi; Pei, Zhijun

doi:10.3727/096504016x14792098307036

Cited by 45 publications

(36 citation statements)

References 26 publications

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“…Clinically, the aberrant overexpression of CASC9 was correlated with the clinical of glioma patients, implying the tumour promoting biomarker of CASC9. More than CASC9, numerous of lncRNAs have been identified to be aberrantly overexpressed in human tumourous tissue, acting as the oncogenic molecular, such as PVT1, UCA1, CCAT2 et al Similar to this finding, our results also discover this worthy conclusion.…”

Section: Discussionsupporting

confidence: 85%

Long noncoding RNA CASC9/miR‐519d/STAT3 positive feedback loop facilitate the glioma tumourigenesis

Liu

Yang

et al. 2018

J Cellular Molecular Medi

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Emerging evidence have illustrated the vital roles of long noncoding RNAs (lncRNAs) in glioma. Nevertheless, the majority of their roles and mechanisms in gliomagenesis are still largely unclear. In this study, we investigate the roles of lncRNA CASC9 on glioma tumourigenesis and authenticate its potential mechanisms. Results manifested that CASC9 was highly expressed in glioma specimens and cells, moreover, the ectopic overexpression was correlated with glioma patients’ clinic. Functional studies found that siRNA‐mediated CASC9 silencing inhibited the proliferative ability, invasion in vitro, and impaired the tumour growth in vivo. Mechanical studies revealed that miR‐519d both targeted the 3′‐UTR of CASC9 and STAT3 mRNA, which was identified by luciferase reporter assay and RNA immunoprecipitation (RIP). Moreover, chromatin immunoprecipitation (ChIP) and luciferase reporter assay revealed that STAT3, an oncogenic transcription factor, could bind with the promoter of CASC9 and activate its transcriptional level. In conclusion, our results concluded that CASC9 promotes STAT3 expression via sponging miR‐519d, in return, STAT3 activate CASC9 transcription, forming a positive feedback loop of CASC9/miR‐519d/STAT3. The novel finding provides a potential therapeutic target for glioma.

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Section: Discussionsupporting

confidence: 85%

Long noncoding RNA CASC9/miR‐519d/STAT3 positive feedback loop facilitate the glioma tumourigenesis

Liu

Yang

et al. 2018

J Cellular Molecular Medi

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“…For decades, lncRNAs are regarded as the transcription “noise,” therefore, no further studies are contributed to the research. LncRNAs also regulate the tumor stem cell characteristics (Qin, Tong, Sun, & Xu, ; Zeng et al, ). For example, lncRNA HOTTIP is over‐expressed in human pancreatic cancer and HOTTIP variation regulates the pancreatic cancer stemness factors (LIN28, NANOG, OCT4, and SOX2) and stem markers (ALDH1, CD44, and CD133) by regulating HOXA9 and enhancing the Wnt/β‐catenin pathway by binding with WDR5 (Fu et al, ).…”

Section: Introductionmentioning

confidence: 99%

Long non‐coding RNA FEZF1‐AS1 promotes breast cancer stemness and tumorigenesis via targeting miR‐30a/Nanog axis

Zhang

Sun²,

Zhang³

et al. 2018

Journal Cellular Physiology

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Long non-coding RNAs (lncRNAs) have been verified to modulate the tumorigenesis of breast cancer at multiple levels. In present study, we aim to investigate the role of lncRNA FEZF1-AS1 on breast cancer-stem like cells (BCSC) and the potential regulatory mechanism. In breast cancer tissue, lncRNA FEZF1-AS1 was up-regulated compared with controls and indicated poor prognosis of breast cancer patients. In vitro experiments, FEZF1-AS1 was significantly over-expressed in breast cancer cells, especially in sphere subpopulation compared with parental subpopulation. Loss-of-functional indicated that, in BCSC cells (MDA-MB-231 CSC, MCF-7 CSC), FEZF1-AS1 knockdown reduced the CD44 /CD24 rate, the mammosphere-forming ability, stem factors (Nanog, Oct4, SOX2), and inhibited the proliferation, migration and invasion. In vivo, FEZF1-AS1 knockdown inhibited the breast cancer cells growth. Bioinformatics analysis tools and series of validation experiments confirmed that FEZF1-AS1 modulated BCSC and Nanog expression through sponging miR-30a, suggesting the regulation of FEZF1-AS1/miR-30a/Nanog. In summary, our study validate the important role of FEZF1-AS1/miR-30a/Nanog in breast cancer stemness and tumorigenesis, providing a novel insight and treatment strategy for breast cancer.

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“…26 Up to date, a plethora of lncRNAs have been certified to participate in mediating glioma metastasis, including lncRNA UCA1, 27 lncRNA H19, 28 lncRNA HOTTIP, 29 lncRNA CCAT1 30 and lncRNA CCAT2. 13 The current investigation placed the emphasis on lncRNA CCAT2, whose expressional change could reflect glioma onset and prognosis (Tables 2 and 3, Figure 1C). Mechanically, an expressional increase of CCAT2 was found to enable glioma cells to migrate and invade more aggressively than control cells (Figure 4).…”

Section: Discussionmentioning

confidence: 99%

“…12 Zeng and his colleagues also portrayed that there was huge potential for CCAT2 to strengthen epithelial-mesenchymal transition (EMT) and proliferation of glioma cells. 13 Though a direct correlation was displayed between CCAT2 and glioma progression, signaling that CCAT2 functioned on and the association of CCAT2 with chemoresistance of glioma cells remained uncertain.…”

Section: Introductionmentioning

confidence: 99%

<p>lncRNA CCAT2 Enhanced Resistance of Glioma Cells Against Chemodrugs by Disturbing the Normal Function of miR-424</p>

Ding¹,

Zhang²,

Chen³

et al. 2020

OTT

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These authors contributed equally to this workBackground: Aggressive metastasis of tumor cells assumed a constructive role in strengthening chemoresistance of tumors, so this investigation was intended to elucidate if lncRNA CCAT2 sponging downstream miR-424 regulated chemotolerance of glioma cells by boosting metastasis of glioma cells. Methods: One hundred and twenty-eight pairs of glioma tissues and corresponding adjacent tissues were resected from glioma patients during their operation, and we also purchased a series of glioma cell lines, including U251, U87, A172 and SHG44. Furthermore, pcDNA3.1-CCAT2, si-CCAT2, miR-424 mimic and miR-424 inhibitor were transfected into SHG44 and U251 cell lines, so as to evaluate impacts of CCAT2 and miR-424 on chemosensitivity of the glioma cells. Besides, proliferation, invasion and metastasis of the cells were determined through the implementation of colony formation assay, transwell assay and scratch assay. Results: Glioma tissues and cells were monitored with higher CCAT2 expression and lower miR-424 expression than adjacent normal tissues and NHA cell line (P<0.05). Among the glioma cell lines, the SHG44 cell line showed the strongest resistance against teniposide, temozolomide and cisplatin (P<0.05), whereas the U251 cell line was more sensitive to teniposide, temozolomide, vincristine and cisplatin than any other cell line (P<0.05). Besides, pcDNA3.1-CCAT2 and miR-424 inhibitor could enhance tolerance of glioma cell lines against drugs (P<0.05). Moreover, in-vitro transfection of si-CCAT2 and miR-424 mimic could significantly retard proliferation, invasion and migration of SHG44 and U251 cells (P<0.05), and CCAT2 was found to negatively regulate miR-424 expression by sponging it (P<0.05). In addition, CHK1 was deemed as the molecule targeted by upstream miR-424, and its overexpression can changeover the effects of miR-424 mimic on proliferation and metastasis of SHG44 and U251 cells. Conclusion: lncRNA CCAT2/miR-424/Chk1 axis might serve as a promising target for improving chemotherapeutic efficacies in glioma treatment.

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Knockdown of Long Noncoding RNA CCAT2 Inhibits Cellular Proliferation, Invasion, and Epithelial‐Mesenchymal Transition in Glioma Cells

Cited by 45 publications

References 26 publications

Long noncoding RNA CASC9/miR‐519d/STAT3 positive feedback loop facilitate the glioma tumourigenesis

Long noncoding RNA CASC9/miR‐519d/STAT3 positive feedback loop facilitate the glioma tumourigenesis

Long non‐coding RNA FEZF1‐AS1 promotes breast cancer stemness and tumorigenesis via targeting miR‐30a/Nanog axis

<p>lncRNA CCAT2 Enhanced Resistance of Glioma Cells Against Chemodrugs by Disturbing the Normal Function of miR-424</p>

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