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dc.contributor.authorKasama, Hiroki
dc.contributor.authorSakamoto, Yosuke
dc.contributor.authorKasamatsu, Atsushi
dc.contributor.authorOkamoto, Atsushi
dc.contributor.authorKoyama, Tomoyoshi
dc.contributor.authorMinakawa, Yasuyuki
dc.contributor.authorOgawara, Katsunori
dc.contributor.authorYokoe, Hidetaka
dc.contributor.authorShiiba, Masashi
dc.contributor.authorTanzawa, Hideki
dc.contributor.authorUzawa, Katsuhiro
dc.date.accessioned2015-09-01T18:45:23Z
dc.date.available2015-09-01T18:45:23Z
dc.date.issued2015-07-31
dc.identifier.citationBMC Cancer. 2015 Jul 31;15(1):563
dc.identifier.urihttp://dx.doi.org/10.1186/s12885-015-1577-2
dc.identifier.urihttp://hdl.handle.net/10724/32064
dc.description.abstractAbstract Background Adenosine A2b receptor (ADORA2B) encodes an adenosine receptor that is a member of the G protein-coupled receptor superfamily. This integral membrane protein stimulates adenylate cyclase activity in the presence of adenosine. Little is known about the relevance of ADORA2B to human malignancy including oral squamous cell carcinoma (OSCC). We aimed to characterize the expression state and function of ADORA2B in OSCC. Methods The ADORA2B expression levels in nine OSCC-derived cells were analyzed by quantitative reverse transcriptase-polymerase chain reaction and immunoblotting analyses. Using an ADORA2B knockdown model, we assessed cellular proliferation and expression of hypoxia-inducible factor1α (HIF-1α). We examined the adenosine receptor expression profile under both normoxic and hypoxic conditions in the OSCC-derived cells. In addition to in vitro data, the clinical correlation between the ADORA2B expression levels in primary OSCCs (n = 100 patients) and the clinicopathological status by immunohistochemistry (IHC) also was evaluated. Results ADORA2B mRNA and protein were up-regulated significantly (p < 0.05) in seven OSCC-derived cells compared with human normal oral keratinocytes. Suppression of ADORA2B expression with shRNA significantly (p < 0.05) inhibited cellular proliferation compared with the control cells. HIF-1α also was down-regulated in ADORA2B knockdown OSCC cells. During hypoxia, ADORA2B expression was induced significantly (p < 0.05) in the mRNA and protein after 24 hours of incubation in OSCC-derived cells. IHC showed that ADORA2B expression in primary OSCCs was significantly (p < 0.05) greater than in the normal oral counterparts and that ADORA2B-positive OSCCs were correlated closely (p < 0.05) with tumoral size. Conclusion Our results suggested that ADORA2B controls cellular proliferation via HIF-1α activation, indicating that ADORA2B may be a key regulator of tumoral progression in OSCCs.
dc.titleAdenosine A2b receptor promotes progression of human oral cancer
dc.typeJournal Article
dc.date.updated2015-07-31T03:48:44Z
dc.language.rfc3066en
dc.rights.holderKasama et al.


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