PMID- 29039609 OWN - NLM STAT- MEDLINE DCOM- 20180720 LR - 20181113 IS - 1791-2431 (Electronic) IS - 1021-335X (Print) IS - 1021-335X (Linking) VI - 38 IP - 6 DP - 2017 Dec TI - Quercetrin from Toona sinensis leaves induces cell cycle arrest and apoptosis via enhancement of oxidative stress in human colorectal cancer SW620 cells. PG - 3319-3326 LID - 10.3892/or.2017.6042 [doi] AB - Finding effective strategies against colorectal cancer (CRC) is still an emergent health problem. In the present study, we investigated the anticancer activity of quercetrin from Toona sinensis leaves (QTL) and explored the underlying mechanism in human CRC cell line SW620. The cells were treated with various concentrations of QTL and the cytotoxic effects of QTL were determined using the MTT assay. Apoptosis and cell cycle status were detected by flow cytometry. Reactive oxygen species (ROS) levels and mitochondrial membrane potential (∆Psim) were assessed using DCF-DA and JC-1 fluorescence spectrophotometry, respectively. Western blot analysis was used to quantify the expression of apoptosis‑related proteins. RT-PCR was applied to determine the mRNA levels of glutathione peroxidase (GPx) and catalase (CAT). QTL exhibited growth inhibitory effects and caused cell cycle arrest in the G2/M phase, which was accompanied by increased expression of p53 and p21 proteins. QTL promoted apoptosis which was consistent with the upregulated expression of Bax, cytochrome c, caspase-9, Apaf-1 and caspase-3. In addition, QTL induced the loss of mitochondrial membrane potential and triggered ROS generation, as revealed by the downregulated mRNA expression and enzymatic activity of GPx and CAT. Furthermore, both N‑acetyl cysteine (NAC) and GSH attenuated the QTL-induced growth inhibition observed in SW620 cells along with the increase of ROS levels. These findings revealed that QTL inhibited the growth of CRC cells and facilitated apoptosis by enhancing oxidative stress. QTL may therefore have potential for use in CRC chemotherapy. FAU - Zhang, Yali AU - Zhang Y AD - Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi 710049, P.R. China. FAU - Guo, Yucheng AU - Guo Y AD - Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi 710049, P.R. China. FAU - Wang, Mimi AU - Wang M AD - Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi 710049, P.R. China. FAU - Dong, Huanhuan AU - Dong H AD - Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi 710049, P.R. China. FAU - Zhang, Jingfang AU - Zhang J AD - College of Forestry, Northwest A&F University, Yangling, Shaanxi 712100, P.R. China. FAU - Zhang, Liyu AU - Zhang L AD - Shaanxi Institute of Pediatric Diseases, Xi'an Children's Hospital, Xi'an, Shaanxi 710049, P.R. China. LA - eng PT - Journal Article DEP - 20171017 PL - Greece TA - Oncol Rep JT - Oncology reports JID - 9422756 RN - 0 (APAF1 protein, human) RN - 0 (Apoptotic Protease-Activating Factor 1) RN - 0 (Plant Extracts) RN - 0 (Reactive Oxygen Species) RN - 2Y8906LC5P (quercitrin) RN - 9IKM0I5T1E (Quercetin) RN - EC 1.11.1.9 (Glutathione Peroxidase) RN - EC 3.4.22.- (Caspase 3) SB - IM MH - Apoptosis/drug effects MH - Apoptotic Protease-Activating Factor 1/genetics MH - Caspase 3/genetics MH - Cell Cycle Checkpoints/drug effects MH - Cell Line, Tumor MH - Cell Proliferation/drug effects MH - Colorectal Neoplasms/*drug therapy/genetics/pathology MH - Gene Expression Regulation, Neoplastic/drug effects MH - Glutathione Peroxidase/genetics MH - Humans MH - Meliaceae/chemistry MH - Membrane Potential, Mitochondrial/drug effects MH - Oxidative Stress/*drug effects MH - Plant Extracts/*administration & dosage/chemistry MH - Quercetin/administration & dosage/*analogs & derivatives/chemistry MH - Reactive Oxygen Species/metabolism PMC - PMC5783577 EDAT- 2017/10/19 06:00 MHDA- 2018/07/22 06:00 PMCR- 2017/10/17 CRDT- 2017/10/18 06:00 PHST- 2017/04/01 00:00 [received] PHST- 2017/09/15 00:00 [accepted] PHST- 2017/10/19 06:00 [pubmed] PHST- 2018/07/22 06:00 [medline] PHST- 2017/10/18 06:00 [entrez] PHST- 2017/10/17 00:00 [pmc-release] AID - or-38-06-3319 [pii] AID - 10.3892/or.2017.6042 [doi] PST - ppublish SO - Oncol Rep. 2017 Dec;38(6):3319-3326. doi: 10.3892/or.2017.6042. Epub 2017 Oct 17.