背景:乳腺癌,在人类中被称为乳腺癌,来自乳腺中攻击周围组织的细胞异常生长的结果。分子水平的致癌过程可以通过作为致癌生物标志物的蛋白质的产生来监测。7,12-二甲基苯并[a]蒽(DMBA)是已知的致癌化合物。这项研究旨在分析蛋白质组学概况,作为有关Sprague-Dawley大鼠中DMBA诱导的致癌作用的关键数据。方法:实验动物分为两组:治疗组给予DMBA,剂量为10mg/kg(乳房内),间隔48小时,共10剂,阴性对照组不给予任何治疗。使用分光光度计进行总蛋白质浓度的测量。并使用t检验对数据进行分析,而蛋白质谱的表征是基于分子量数据使用SDS-PAGE进行的。通过苏木精和曙红(H&E)染色评价乳腺组织病理学。结果:结果显示大鼠乳腺癌模型中总蛋白浓度显著(p<0.05)增加27%。蛋白质组学表征的结果表明,含有187、169、68、64、53、41、24、18和14kDa的蛋白质的蛋白质谱,怀疑是她的2号,尼沙林,COX-2,白蛋白,Vimentin,ACTB,TNF,p16和脂肪酸结合蛋白3(FABP3),分别。乳腺的组织病理学显示肺泡的不规则和模糊排列以及从表面到乳腺管腔的广泛上皮细胞增殖,乳腺基质显示了新的上皮细胞的形成,癌细胞扩散到周围组织。结论:在DMBA诱导的乳腺癌大鼠模型中,蛋白质组学特征与乳腺癌发生的形态学改变密切相关。
Background: Mammary cancer, called breast cancer in humans, results from the abnormal growth of cells in the mammary glands that attack the surrounding tissue. The process of carcinogenesis at the molecular level can be monitored through the production of proteins as biomarkers for carcinogenesis. 7,12-Dimethylbenz[a]anthracene (DMBA) is a known carcinogenic compound. This study aimed to analyze the proteomic profile as critical data regarding DMBA-induced carcinogenesis in Sprague‒Dawley rats. Methods: Experimental animals were divided into two groups: a treatment group given DMBA at a dose of 10 mg/kg (intramammary) at intervals of 48 hours for a total of 10 doses, and a negative control group that was not given any treatment. Measurement of the total protein concentration was carried out using a spectrophotometer, and the data were analyzed using a t-test, while the characterization of protein profiles was carried out based on molecular weight data using SDS‒PAGE. Mammary gland histopathology was evaluated by hematoxylin and eosin (H&E) staining. Results: The results showed a significant (p<0.05) increase of 27% in the total protein concentration in the rat mammary cancer model. The results of proteomic characterization showed a protein profile containing proteins of 187, 169, 68, 64, 53, 41, 24, 18, and 14 kDa, which were suspected to be HER-2, Nischarin, COX-2, Albumine, Vimentin, ACTB, TNF, p16, and fatty acid binding protein 3 (FABP3), respectively. Histopathology of the mammary glands showed an irregular and indistinct arrangement of the alveoli and extensive epithelial cell proliferation from the surface to the lumen of the mammary ducts, and the mammary stroma showed the formation of new epithelial cells, which were cancer cells that spread to surrounding tissue. Conclusions: The proteomic profile was strongly associated with morphological alterations in mammary carcinogenesis in a rat model of DMBA-induced mammary cancer.