Please use this identifier to cite or link to this item: https://doi.org/10.3390/biom9070253
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dc.titleIsoform-specific role of akt in oral squamous cell carcinoma
dc.contributor.authorRoy, N.K.
dc.contributor.authorMonisha, J.
dc.contributor.authorPadmavathi, G.
dc.contributor.authorLalhruaitluanga, H.
dc.contributor.authorKumar, N.S.
dc.contributor.authorSingh, A.K.
dc.contributor.authorBordoloi, D.
dc.contributor.authorBaruah, M.N.
dc.contributor.authorAhmed, G.N.
dc.contributor.authorLongkumar, I.
dc.contributor.authorArfuso, F.
dc.contributor.authorKumar, A.P.
dc.contributor.authorKunnumakkara, A.B.
dc.date.accessioned2021-12-06T04:23:50Z
dc.date.available2021-12-06T04:23:50Z
dc.date.issued2019
dc.identifier.citationRoy, N.K., Monisha, J., Padmavathi, G., Lalhruaitluanga, H., Kumar, N.S., Singh, A.K., Bordoloi, D., Baruah, M.N., Ahmed, G.N., Longkumar, I., Arfuso, F., Kumar, A.P., Kunnumakkara, A.B. (2019). Isoform-specific role of akt in oral squamous cell carcinoma. Biomolecules 9 (7) : 253. ScholarBank@NUS Repository. https://doi.org/10.3390/biom9070253
dc.identifier.issn2218-273X
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/209563
dc.description.abstractProtein kinase B (Akt) plays a very significant role in various cancers including oral cancer. However, it has three isoforms (Akt1, Akt2, and Akt3) and they perform distinct functions and even play contrasting roles in different cancers. Therefore, it becomes essential to evaluate the isoform-specific role of Akt in oral cancer. In the present study, an attempt has been made to elucidate the isoform-specific role of Akt in oral cancer. The immunohistochemical analysis of oral cancer tissues showed an overexpression of Akt1 and 2 isoforms but not Akt3. Moreover, the dataset of “The Cancer Genome Atlas” for head and neck cancer has suggested the genetic alterations of Akt1 and 2 tend to be associated with the utmost poor clinical outcome in oral cancer. Further, treatment of oral cancer cells with tobacco and its components such as benzo(a)pyrene and nicotine caused increased mRNA levels of Akt1 and 2 isoforms and also enhanced the aggressiveness of oral cancer cells in terms of proliferation, and clonogenic and migration potential. Finally, silencing of Akt1 and 2 isoforms caused decreased cell survival and induced cell cycle arrest at the G2/M phase. Akt1/2 silencing also reduced tobacco-induced aggressiveness by decreasing the clonogenic and migration potential of oral cancer cells. Moreover, silencing of Akt1 and 2 isoforms was found to decrease the expression of proteins regulating cancer cell survival and proliferation such as cyclooxygenase-2, B-cell lymphoma 2 (Bcl-2), cyclin D1, and survivin. Thus, the important role of Akt1 and 2 isoforms have been elucidated in oral cancer with in-depth mechanistic analysis. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.
dc.publisherMDPI AG
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.sourceScopus OA2019
dc.subjectAkt isoforms
dc.subjectImmunohistochemistry
dc.subjectKnockdown
dc.subjectOral cancer
dc.subjectTissue microarray
dc.subjectTobacco
dc.typeArticle
dc.contributor.departmentCANCER SCIENCE INSTITUTE OF SINGAPORE
dc.description.doi10.3390/biom9070253
dc.description.sourcetitleBiomolecules
dc.description.volume9
dc.description.issue7
dc.description.page253
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