Ashouri Saeideh, Khujin Maryam Hosseindokht, Kazemi Mohammad, Kheirollahi Majid
Department of Genetics and Molecular Biology, Pediatric Inherited Diseases Research Center, Research Institute for Primordial Prevention of Noncommunicable Disease, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Adv Biomed Res. 2016 Nov 28;5:172. doi: 10.4103/2277-9175.190984. eCollection 2016.
Teicoplanin is a member of vancomycin-ristocetin family of glycopeptide antibiotics. It mediated wound healing by increasing neovascularization possibly through activation of MAP kinase signaling pathway. The aim of this study is an evaluation of c-myc and c-fos genes expression after treatment of cells by teicoplanin and determines whether this glycopeptide antibiotic exerts its proliferation effects by influencing the expression of these genes. Hence, this study was designed to elucidate one possible mechanism underlying teicoplanin effects on cell proliferation using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay.
Breast cancer cell line, MCF-7, was cultured, and three different concentrations of teicoplanin were added to the plates. We measured the cell proliferation rate by MTT assay. After cell harvesting, total RNA was extracted to synthesize single-stranded cDNA. Real-time polymerase chain reaction was performed, and the data were analyzed.
It was observed that the level of c-fos and c-myc genes' expressions was decreased at all three different concentrations of teicoplanin.
it could be concluded that although teicoplanin is considered as an enhancing cell growth and proliferation, but probably its effect is not through MAP kinase signaling pathway or perhaps even has inhibitory effect on the expression of some genes such as c-myc and c-fos in this pathway. Hence, the mechanism of action of teicoplanin for increasing cell propagation, through cell signaling pathways or chromosomal abnormalities, remains unclear, and further studies should be conducted.
替考拉宁是糖肽类抗生素万古霉素-瑞斯托菌素家族的成员。它可能通过激活丝裂原活化蛋白激酶(MAP)信号通路增加新血管形成,从而介导伤口愈合。本研究的目的是评估替考拉宁处理细胞后c-myc和c-fos基因的表达,并确定这种糖肽类抗生素是否通过影响这些基因的表达发挥其增殖作用。因此,本研究旨在使用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基-2H-四唑溴盐(MTT)法阐明替考拉宁对细胞增殖作用的一种可能机制。
培养乳腺癌细胞系MCF-7,并向培养板中加入三种不同浓度的替考拉宁。我们通过MTT法测量细胞增殖率。细胞收获后,提取总RNA以合成单链cDNA。进行实时聚合酶链反应,并对数据进行分析。
观察到在三种不同浓度的替考拉宁作用下,c-fos和c-myc基因的表达水平均降低。
可以得出结论,尽管替考拉宁被认为具有促进细胞生长和增殖的作用,但其作用可能并非通过MAP激酶信号通路,甚至可能对该通路中的某些基因如c-myc和c-fos的表达具有抑制作用。因此,替考拉宁通过细胞信号通路或染色体异常增加细胞增殖的作用机制仍不清楚,需要进一步研究。