PMID- 28092843 OWN - NLM STAT- MEDLINE DCOM- 20170327 LR - 20170327 IS - 1950-6007 (Electronic) IS - 0753-3322 (Linking) VI - 88 DP - 2017 Apr TI - Therapeutic effects of bach1 siRNA on human breast adenocarcinoma cell line. PG - 34-42 LID - S0753-3322(16)31634-1 [pii] LID - 10.1016/j.biopha.2017.01.030 [doi] AB - BACKGROUND: Despite the great improvements in clinical and therapeutic techniques in recent years, many advanced breast cancer patients still died of the postoperative recurrence and metastasis of disease. Bach1 plays a role in the development of the invasive phenotypes of cancer, cell division and apoptosis in tumor cells. The aim of this study was to investigate the effect of specific bach1 siRNAs, on the proliferation, migration, invasive, induction of apoptosis, cell cycle arrest and alter EMT related miRNA of MDA-MB-468 cells (breast cancer). METHODS: siRNA transfection was performed with transfection reagent. The expression levels of Bach1 mRNA and protein were measured by qRT-PCR and western blot analysis, respectively. The survival of cells was determined using MTT assay cells, apoptosis using Tunel assay, Cell migration using scratch assay and Cell cycle analysis by Propidium Iodide (PI) DNA staining method by using flow cytometry on the MDA-MB-468. The expression levels of MMP-9 and CXCR4 were measured by qRT-PCR. RESULTS: Transfection with siRNA significantly suppressed the expression of bach1 gene in dose dependent manner after 48h (p<0.0001). Surprisingly, treatment with bach1 siRNA arrest cell cycle in S phases (p<0.0001). Moreover siRNA transfection had effects on breast adenocarcinoma cells and inhibits the migration (p<0.0001), proliferation (p<0.0001), cell cycle arrest (p=0.03) and induces apoptosis (p<0.0001) and reduces the expression of miR-21 (P=0.0014). CONCLUSION: Our results suggest that the bach1 can be considered as a potent adjuvant in breast cancer therapy. CI - Copyright (c) 2017 Elsevier Masson SAS. All rights reserved. FAU - Aletaha, Mansoor AU - Aletaha M AD - Biotechnology, Department of Pathobiology, Shiraz University, Shiraz, Iran. FAU - Mansoori, Behzad AU - Mansoori B AD - Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. FAU - Mohammadi, Ali AU - Mohammadi A AD - Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. FAU - Fazeli, Mehdi AU - Fazeli M AD - Department of Pharmacology and Toxicology, School of Veterinary Medicine, Shiraz University, Shiraz, Iran. FAU - Baradaran, Behzad AU - Baradaran B AD - Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Electronic address: behzad_im@yahoo.com. LA - eng PT - Journal Article DEP - 20170113 PL - France TA - Biomed Pharmacother JT - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie JID - 8213295 RN - 0 (BACH1 protein, human) RN - 0 (Basic-Leucine Zipper Transcription Factors) RN - 0 (CXCR4 protein, human) RN - 0 (Fanconi Anemia Complementation Group Proteins) RN - 0 (MIRN21 microRNA, human) RN - 0 (MicroRNAs) RN - 0 (RNA, Messenger) RN - 0 (RNA, Small Interfering) RN - 0 (Receptors, CXCR4) RN - EC 3.4.24.35 (Matrix Metalloproteinase 9) SB - IM MH - Adenocarcinoma/*genetics/pathology MH - Apoptosis/genetics MH - Basic-Leucine Zipper Transcription Factors/genetics/*metabolism MH - Breast Neoplasms/*genetics/pathology MH - Cell Cycle Checkpoints/genetics MH - Cell Line, Tumor MH - Cell Movement/genetics MH - Cell Proliferation MH - Fanconi Anemia Complementation Group Proteins/genetics/*metabolism MH - Female MH - Gene Expression Regulation, Neoplastic MH - Gene Knockdown Techniques MH - Gene Silencing MH - Humans MH - Matrix Metalloproteinase 9/genetics/metabolism MH - MicroRNAs/genetics/metabolism MH - Neoplasm Metastasis MH - RNA, Messenger/genetics/metabolism MH - RNA, Small Interfering/*therapeutic use MH - Receptors, CXCR4/genetics/metabolism MH - Transfection OTO - NOTNLM OT - Bach1 OT - Breast cancer OT - MDA-MB-468 OT - RNA interference OT - siRNA EDAT- 2017/01/17 06:00 MHDA- 2017/03/28 06:00 CRDT- 2017/01/17 06:00 PHST- 2016/09/17 00:00 [received] PHST- 2017/01/05 00:00 [accepted] PHST- 2017/01/17 06:00 [pubmed] PHST- 2017/03/28 06:00 [medline] PHST- 2017/01/17 06:00 [entrez] AID - S0753-3322(16)31634-1 [pii] AID - 10.1016/j.biopha.2017.01.030 [doi] PST - ppublish SO - Biomed Pharmacother. 2017 Apr;88:34-42. doi: 10.1016/j.biopha.2017.01.030. Epub 2017 Jan 13.