Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/91665
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dc.contributorDepartment of Health Technology and Informatics-
dc.creatorKhan, MZI-
dc.creatorLaw, HKW-
dc.date.accessioned2021-11-24T06:07:29Z-
dc.date.available2021-11-24T06:07:29Z-
dc.identifier.urihttp://hdl.handle.net/10397/91665-
dc.language.isoenen_US
dc.publisherBioMed Centralen_US
dc.rights© The Author(s) 2021.en_US
dc.rightsThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.en_US
dc.rightsThe following publication Islam Khan, M.Z., Law, H.K.W. RAMS11 promotes CRC through mTOR-dependent inhibition of autophagy, suppression of apoptosis, and promotion of epithelial-mesenchymal transition. Cancer Cell Int 21, 321 (2021) is available at https://doi.org/10.1186/s12935-021-02023-6en_US
dc.subjectLncRNAsen_US
dc.subjectRAMS11en_US
dc.subjectCRCen_US
dc.subjectAutophagyen_US
dc.subjectApoptosisen_US
dc.subjectEMTen_US
dc.titleRAMS11 promotes CRC through mTOR-dependent inhibition of autophagy, suppression of apoptosis, and promotion of epithelial-mesenchymal transitionen_US
dc.typeJournal/Magazine Articleen_US
dc.identifier.volume21-
dc.identifier.issue1-
dc.identifier.doi10.1186/s12935-021-02023-6-
dcterms.abstractBackground Long non-coding RNAs (lncRNAs), a class of non-coding RNAs (ncRNAs) associated with diverse biological processes of cells. Over the past decades, cumulating research evidences revealed that abnormal expressions of lncRNAs are associated with colorectal cancer (CRC) initiation, progression, metastasis, and resistance to therapies. Moreover, their usefulness as candidate biomarkers for CRC diagnosis and prognosis are well evident throughout previous literature. In the current study, we examined the role and molecular mechanisms of newly identified lncRNA named RNA associated with metastasis-11 (RAMS11) in CRC development. Methods The expression of RAMS11 in CRC cell lines DLD-1, HT-29, HCT-116, and SW480 and colon normal cells CCD-112-CoN were evaluated by quantitative RT-qPCR. The results showed that the RAMS11 is significantly upregulated in CRC cell lines compared to the normal cells. The CCK-8 proliferation assay, colony formation assay, and migration assay were performed to evaluate the biological and physiological functions of RAMS11 in vitro. To decipher the molecular mechanisms of RAMS11 medicated CRC progression, we further performed western blot analysis of the key pathway proteins (e.g., AMPK, AKT, and mTOR). Results Our results revealed that higher expression of RAMS11 is associated with increased CRC proliferation, migration, and development of metastasis. Knockdown of RAMS11 induced autophagy, apoptosis along with reduction of epithelial-mesenchymal transition (EMT) suggesting that RAMS11 is involved in CRC progression. The molecular mechanisms of RAMS11 indicated that knockdown of RAMS11 significantly inhibited CRC carcinogenesis through mTOR-dependent autophagy induction. Conclusions In sum, our results suggested that RAMS11 is an important oncogene in CRC pathogenesis. Targeting RAMS11 could be a potential therapeutic strategy for CRC management.-
dcterms.accessRightsopen accessen_US
dcterms.bibliographicCitationCancer cell international, 2021, v. 21, no. 1, 321-
dcterms.isPartOfCancer cell international-
dcterms.issued2021-
dc.identifier.isiWOS:000668579900002-
dc.identifier.pmid34174900-
dc.identifier.eissn1475-2867-
dc.identifier.artn321-
dc.description.validate202111 bchy-
dc.description.oaVersion of Recorden_US
dc.identifier.FolderNumberOA_Scopus/WOSen_US
dc.description.pubStatusPublisheden_US
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