000062020 001__ 62020
000062020 005__ 20210310171107.0
000062020 0247_ $$2doi$$a10.3389/fphar.2017.00321
000062020 0248_ $$2sideral$$a101072
000062020 037__ $$aART-2017-101072
000062020 041__ $$aeng
000062020 100__ $$aJiménez, Pilar
000062020 245__ $$aCD24 expression is increased in 5-fluorouracil-treated esophageal adenocarcinoma cells
000062020 260__ $$c2017
000062020 5060_ $$aAccess copy available to the general public$$fUnrestricted
000062020 5203_ $$ahe cancer stem cell (CSC) model suggests that there are subsets of cells within a tumor with increased proliferation and self-renewal capacity, which play a key role in therapeutic resistance. The importance of cyclooxygenase-2 (COX-2) in carcinogenesis has been previously established and the use of COX-2 inhibitors as celecoxib has been shown to exert antitumor effects. The present study investigated whether treatment of esophageal adenocarcinoma (EAC) cells with 5-fluorouracil (5-FU) or the growth of tumor spheres increased the proportion of CSCs and also if treatment with celecoxib was able to reduce the putative CSC markers in this tumor. OE19 and OE33 EAC cells surviving 5-FU exposure exhibited an increase in CSC markers CD24 and ABCG2 and also an increased resistance to apoptosis. EAC cell lines had the capacity to form multiple spheres displaying typical CSC functionalities such as self-renewal and increased CD24 levels. In addition, after the induction of differentiation, cancer cells reached levels of CD24 similar to those observed in the parental cells. Treatment with celecoxib alone or in combination with 5-FU also resulted in a reduction of CD24 expression. Moreover, celecoxib inhibited the growth of tumor spheres. These findings showing a reduction in CSC markers induced by celecoxib suggest that the COX-2 inhibitor might be a candidate for combined chemotherapy in the treatment of EAC. However, additional clinical and experimental studies are needed.
000062020 536__ $$9info:eu-repo/grantAgreement/ES/IACS/PIPAMER-07-08$$9info:eu-repo/grantAgreement/ES/IACS/PIPAMER-08-12
000062020 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/
000062020 590__ $$a3.831$$b2017
000062020 591__ $$aPHARMACOLOGY & PHARMACY$$b48 / 261 = 0.184$$c2017$$dQ1$$eT1
000062020 592__ $$a1.587$$b2017
000062020 593__ $$aPharmacology (medical)$$c2017$$dQ1
000062020 593__ $$aPharmacology$$c2017$$dQ1
000062020 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000062020 700__ $$aChueca, Eduardo
000062020 700__ $$aArruebo, María
000062020 700__ $$aStrunk, Mark
000062020 700__ $$0(orcid)0000-0001-8056-5236$$aSolanas, Estela$$uUniversidad de Zaragoza
000062020 700__ $$0(orcid)0000-0002-7119-2244$$aSerrano, Trinidad$$uUniversidad de Zaragoza
000062020 700__ $$aGarcía-González, María A.
000062020 700__ $$0(orcid)0000-0001-5932-2889$$aLanas, Ángel$$uUniversidad de Zaragoza
000062020 7102_ $$11003$$2443$$aUniversidad de Zaragoza$$bDpto. Anatom.Histolog.Humanas$$cArea Histología
000062020 7102_ $$11007$$2610$$aUniversidad de Zaragoza$$bDpto. Medicina, Psiqu. y Derm.$$cArea Medicina
000062020 773__ $$g8 (2017), [11 pp]$$pFront. pharmacol.$$tFrontiers in pharmacology$$x1663-9812
000062020 8564_ $$s1736001$$uhttps://zaguan.unizar.es/record/62020/files/texto_completo.pdf$$yVersión publicada
000062020 8564_ $$s11477$$uhttps://zaguan.unizar.es/record/62020/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000062020 909CO $$ooai:zaguan.unizar.es:62020$$particulos$$pdriver
000062020 951__ $$a2021-03-10-17:00:47
000062020 980__ $$aARTICLE