Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/89794
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dc.contributorDepartment of Health Technology and Informaticsen_US
dc.creatorIslam Khan, MZen_US
dc.creatorLaw, HKWen_US
dc.date.accessioned2021-05-11T02:17:33Z-
dc.date.available2021-05-11T02:17:33Z-
dc.identifier.urihttp://hdl.handle.net/10397/89794-
dc.language.isoenen_US
dc.publisherFrontiers Research Foundationen_US
dc.rightsCopyright © 2021 Islam Khan and Law. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.en_US
dc.subjectCancer susceptibility candidate 9en_US
dc.subjectLong non-coding RNAen_US
dc.subjectColorectal canceren_US
dc.subjectAutophagyen_US
dc.subjectEpithelialmesenchymal transitionen_US
dc.titleCancer susceptibility candidate 9 (CASC9) promotes colorectal cancer carcinogenesis via mTOR-dependent autophagy and epithelial–mesenchymal transition pathwaysen_US
dc.typeJournal/Magazine Articleen_US
dc.identifier.spage1en_US
dc.identifier.epage12en_US
dc.identifier.volume8en_US
dc.identifier.doi10.3389/fmolb.2021.627022en_US
dcterms.abstractBackground: Colorectal cancer (CRC) is the third most common cancer worldwide. Many recent studies have demonstrated that different long non-coding RNAs (lncRNAs) are involved in the initiation, advancement, and metastasis of many cancers including CRC. Cancer susceptibility candidate 9 (CASC9) is an lncRNA that has been reported in many cancers, but its role in CRC is poorly understood. In this study, we aimed to examine the expression of CASC9 in CRC cell lines and to determine the mechanism of action of CASC9 in CRC carcinogenesis.en_US
dcterms.abstractMethods: The expression of CASC9 in CRC tissues was compared with normal samples from publicly available datasets in The Cancer Genome Atlas (TCGA) and The Encyclopedia of RNA Interactomes (ENCORI). CASC9 expression was further verified in four CRC cell lines (DLD1, HT-29, SW480, and HCT-116) and normal colorectal cell line (CCD-112CoN) by real-time quantitative polymerase chain reaction (RT-qPCR). After gene silencing in HCT-116 and SW480, Cell Counting Kit-8 assay, clonogenic assay, and wound healing assay were performed to evaluate cell proliferation, viability, and migration index of cells. Western blotting was used to explore the key pathways involved.en_US
dcterms.abstractResults: CASC9 was significantly upregulated as analyzed from both public datasets TCGA and ENCORI where its overexpression was associated with poor survival of CRC patients. Similarly, CASC9 was significantly overexpressed in the CRC cell lines compared with normal cells studied. The silencing of CASC9 in HCT-116 and SW480 attenuated cell proliferation and migration significantly. Furthermore, pathways investigations showed that silencing of CASC9 significantly induced autophagy, promoted AMP-activated protein kinase (AMPK) phosphorylation, inhibited mTOR and AKT signaling pathways, and altered epithelial–mesenchymal transition (EMT) marker protein expression.en_US
dcterms.abstractConclusion: We demonstrated that silencing of CASC9 contributes to the reduced CRC cell proliferation and migration by regulating autophagy and AKT/mTOR/EMT signaling. Therefore, CASC9 plays an important role in carcinogenesis, and its expression may act as a prognostic biomarker and a potential therapeutic target of CRC management.en_US
dcterms.accessRightsopen accessen_US
dcterms.bibliographicCitationFrontiers in molecular biosciences, 4 May 2021, v. 8, 627022, p. 1-12en_US
dcterms.isPartOfFrontiers in molecular biosciencesen_US
dcterms.issued2021-05-04-
dc.identifier.scopus2-s2.0-85105978157-
dc.identifier.eissn2296-889Xen_US
dc.identifier.artn627022en_US
dc.description.validate202105 bcwhen_US
dc.description.oaVersion of Recorden_US
dc.identifier.FolderNumbera0882-n01-
dc.identifier.SubFormID2093-
dc.description.fundingSourceOthersen_US
dc.description.fundingTextThis project is partially supported by: (1) Research grant to HKL including Departmental Seeding Fund and Internal Institutional Research Fund (P0031318-UAHS); (2) Postgraduate studentship from The Hong Kong Polytechnic University for ZIK.en_US
dc.description.pubStatusPublisheden_US
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