Pešić, Milica (36768679400)Milica (36768679400)PešićAndjelković, Tijana (55321765700)Tijana (55321765700)AndjelkovićBanković, Jasna (24278374400)Jasna (24278374400)BankovićMarković, Ivanka D. (7004033826)Ivanka D. (7004033826)MarkovićRakić, Ljubiša (35580670800)Ljubiša (35580670800)RakićRuždijić, Sabera (7003935669)Sabera (7003935669)Ruždijić2025-06-122025-06-122009https://doi.org/10.1007/s10637-008-9140-5https://www.scopus.com/inward/record.uri?eid=2-s2.0-66949148061&doi=10.1007%2fs10637-008-9140-5&partnerID=40&md5=55cd2249d92222d8aec82ad964e488c1https://remedy.med.bg.ac.rs/handle/123456789/10532A resistant non-small cell lung carcinoma cell line-NSCLC (NCI-H460/R) was established in order to investigate the potential of sulfinosine (SF) to overcome multidrug resistance (MDR). The cytotoxicity of doxorubicin (DOX) in NCI-H460/R cells was enhanced by interaction with SF. SF improved the sensitivity of resistant cells to DOX when NCI-H460/R cells were pretreated with SF. Synergism was accompanied by the accumulation of cells in S and G 2/M phases. Pretreatment with SF was more potent in improving the sensitivity to DOX than verapamil (VER). The decrease of mdr1 and topo II α expression (assessed by RT-PCR), was consistent with the DOX accumulation assay and cell cycle analysis. Also, SF significantly decreased intracellular glutathione (GSH) concentration. These results point to SF as a potential agent of MDR reversal and a valuable drug for improving chemotherapy of NSCLC. © 2008 Springer Science+Business Media, LLC.DoxorubicinDrug CombinationGlutathioneMultidrug ResistanceNSCLCSulfinosine