TAILIEUCHUNG - Effects of celecoxib and L-NAME on apoptosis and cell cycle of MCF-7 CD44+/CD24-/low subpopulation

Recent studies have reported that cancer stem cells (CSCs) play a pivotal role in treatment failure, causing cancer recurrence. Here, we investigated the effects of L-NAME (an iNOS inhibitor) and celecoxib (a selective COX-2 inhibitor) on CSC-like cells (CSCLCs) and their parental cells. | Turkish Journal of Biology Turk J Biol (2017) 41: 826-834 © TÜBİTAK doi: Research Article Effects of celecoxib and L-NAME on apoptosis and cell cycle of MCF-7 CD44+/CD24–/low subpopulation 1 2 2 1, Maryam MAJDZADEH , Shima ALIEBRAHIMI , Melody VATANKHAH , Seyed Nasser OSTAD * 1 Department of Toxicology and Pharmacology, Faculty of Pharmacy and Poisoning Research Center, Tehran University of Medical Sciences, Tehran, Iran 2 Department of Cellular and Molecular Biology, School of Biology, College of Science, University of Tehran, Tehran, Iran Received: Accepted/Published Online: Final Version: Abstract: Recent studies have reported that cancer stem cells (CSCs) play a pivotal role in treatment failure, causing cancer recurrence. Here, we investigated the effects of L-NAME (an iNOS inhibitor) and celecoxib (a selective COX-2 inhibitor) on CSC-like cells (CSCLCs) and their parental cells. Breast CSC-LCs derived from the MCF-7 cell line were sorted and characterized with the CD44+/CD24–/low phenotype. After isolation, the percentage of the subpopulation expressing CD44+/CD24–/low biomarkers increased considerably from to . Use of L-NAME and celecoxib showed antiproliferative activity towards both MCF-7 and CSC-LCs. Although celecoxib enhanced apoptotic cell death, the CSC-LC population was more resistant than parental cells. Moreover, L-NAME was less effective at inducing apoptosis, suggesting an involvement of different mechanisms of cell death. L-NAME caused cell cycle arrest in the S-phase in CSC-LCs, while celecoxib induced G0/G1 arrest in CSC-LCs and their parental cells. Immunocytochemistry results demonstrated that L-NAME had a similar potency to attenuate iNOS expression in MCF-7 and CSC-LCs; however, celecoxib reduced COX-2 expression in MCF-7 cells. The results show the crucial role of NOS and COX-2 in the maintenance of CD44+/CD24–/low breast .

• Sinh học
• Cancer stem cell like cells
• Breast cancer
• Treatment failure
• iNOS inhibitor
• Parental cells
• BMC Cancer
• Cervical cancer stem cells
• Corresponding parental cells
• Sphere formation
• Non coding RNA molecules
• Cervical cancer
• Cancer cells
• Zebrafish model described
• Human cancer cells
• Metastatic parental cells
• Nonsmall cell lung cancer
• Camphor cytotoxicity
• DNA damaging
• DNA protective
• Drug resistant human lung cancer cell lines
• Quantitative polymerase chain reaction
• Drug treated parental
• Resistant cells
• Tumor suppressor proteins
• BMC Molecular and Cell Biology
• Fetal pig
• Interchromosomal associations
• Insulin like growth factor 2
• Parental specific gene