Long non-coding RNA CASC2 targeting miR-18a suppresses glioblastoma cell growth, metastasis and EMT in vitro and in vivo

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dc.contributor.authorWang, Junen_US
dc.contributor.authorQin, Chaoen_US
dc.contributor.authorZhong, Chenen_US
dc.contributor.authorWen, Yongen_US
dc.contributor.authorKe, Shaen_US
dc.contributor.authorLiao, Boen_US
dc.date.accessioned2020-11-18T10:14:16Z
dc.date.available2020-11-18T10:14:16Z
dc.date.issued2020-08
dc.description.abstractLong non-coding RNAs (lncRNAs) cancer susceptibility candidate 2 (CASC2) has been characterized as atumor suppressor in glioma. Although CASC2 may predict the prognosis of glioma patients, the role andmechanism of CASC2 in human glioblastoma remain to be fully illuminated. Expression of CASC2 and miR18a was detected using RT-qPCR. Cell growth was evaluated by MTT assay, colony formation assay, and flowcytometry; metastasis and epithelial-mesenchymal transition (EMT) were determined with transwell assay andWestern blot, respectively. The target binding between CASC2 and miR-18a was predicted on Starbasesoftware, and confirmed by luciferase reporter assay and RNA immunoprecipitation. Xenograft experimentmeasured tumor growth. As a result, CASC2 was downregulated and miR-18a was upregulated in glioblastomatumor tissues and cells (T98 and A172). Overexpression of CASC2 promoted apoptosis rate and E-cadherinexpression, but suppressed cell viability, colony-forming ability, migration, invasion, and expression ofN-cadherin and Vimentin in T98 and A172 cells, accompanied with tumor growth inhibition in vivo; whereas,silencing of CASC2 exerted the opposite effect on cell growth, metastasis and EMT of T98 and A172 cellsin vitro. However, reintroduction of miR-18a could reverse CASC2 upregulation-mediated suppression onabove cell behaviors in vitro. More importantly, miR-18a was a downstream target for CASC2, and wasnegatively regulated by CASC2. Collectively, this study demonstrated that CASC2 served as tumor suppressorin glioblastoma by inhibiting cell growth, metastasis and EMT both in vitro and in vivo partially via CASC2-miR-18a axis.en_US
dc.identifier.affiliationsDepartment of Neurosurgery, The First People’s Hospital of Changde City, Changde 415000, Hunan, Chinaen_US
dc.identifier.affiliationsDepartment of Neurosurgery, The First People’s Hospital of Changde City, Changde 415000, Hunan, Chinaen_US
dc.identifier.affiliationsDepartment of Neurosurgery, The First People’s Hospital of Changde City, Changde 415000, Hunan, Chinaen_US
dc.identifier.affiliationsDepartment of Neurosurgery, The First People’s Hospital of Changde City, Changde 415000, Hunan, Chinaen_US
dc.identifier.affiliationsDepartment of Neurology, The Affiliated Hospital of North Sichuan Medical College, Nanchong 637000, Sichuan, Chinaen_US
dc.identifier.affiliationsDepartment of Neurology, The Affiliated Hospital of North Sichuan Medical College, Nanchong 637000, Sichuan, Chinaen_US
dc.identifier.citationWang Jun, Qin Chao, Zhong Chen, Wen Yong, Ke Sha, Liao Bo. Long non-coding RNA CASC2 targeting miR-18a suppresses glioblastoma cell growth, metastasis and EMT in vitro and in vivo. Journal of Biosciences. 2020 Aug; : 1-14en_US
dc.identifier.issn0250-5991
dc.identifier.issn0973-7138
dc.identifier.placeIndiaen_US
dc.identifier.urihttps://imsear.searo.who.int/handle/123456789/214249
dc.languageenen_US
dc.publisherIndian Academy of Sciencesen_US
dc.relation.volume45en_US
dc.source.urihttps://dx.doi.org//10.1007/s12038-020-00077-8en_US
dc.subjectCASC2en_US
dc.subjectcell growthen_US
dc.subjectEMTen_US
dc.subjectglioblastomaen_US
dc.subjectmetastasisen_US
dc.subjectmiR-18aen_US
dc.titleLong non-coding RNA CASC2 targeting miR-18a suppresses glioblastoma cell growth, metastasis and EMT in vitro and in vivoen_US
dc.typeJournal Articleen_US
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