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作 者:谢雪娇[1] 栾生[1] 王媛[1] 张莉[1] 崔英俊[1] 王春梅[1] 李庆章[1]
机构地区:[1]东北农业大学乳品科学教育部重点实验室,哈尔滨150030
出 处:《中国畜牧兽医》2015年第7期1680-1685,共6页China Animal Husbandry & Veterinary Medicine
基 金:黑龙江省教育厅重点项目(1154z1004)
摘 要:MicroRNAs(miRNAs)是一类长度约为22nt的非编码的调控性小RNA,在诸多生命活动中发挥重要作用,如参与调控细胞的增殖、分化、凋亡及肿瘤的发生发展。本试验应用脂质体转染技术抑制miR-142-3p在人乳腺上皮细胞的表达。试验采用实时荧光定量PCR、Western blotting、细胞增殖分析等技术,探索miR-142-3p对人乳腺上皮细胞增殖及乳蛋白合成的影响。结果显示,miR-142-3p沉默后,催乳素受体(prolactin receptor,PRLR)蛋白表达增强,同时,相关通路蛋白AKT、mTOR、STAT5、cyclinD1表达量均增加,细胞增殖能力增强。结果表明,在人乳腺上皮细胞中,miR-142-3p的沉默使PRLR蛋白表达量升高,通过调控AKT、mTOR、STAT5、cyclinD1相关通路蛋白而促进乳蛋白质的合成和乳腺上皮细胞的增殖。MicroRNAs (miRNAs) are a group of small,non-coding RNA molecules about 22 nu- cleotides to regulate a wide variety of important biological processes,including cell proliferation, differentiation,apoptosis as well as the progression of tumors. Liposome transfection was used to detect the expression of miR-142-3p in human mammary epithelial cells,the effects of miR-142-3p on the cell proliferation, apoptosis and milk protein synthesis were detected by Real-time PCR, Western blotting,cell proliferation analysis. The results indicated that after miR-142-3p being si- lenced,prolactin receptor (PRLR) protein was increased,at the same time the expressions of re- lated pathways protein AKT,mTOR,STAT5 and cyclinD1 were increased,the ability of cell pro- liferation was increased. The results suggested that in human mammary epithelial cells, the silence of miR-142-3p could increase the expression of PRLR protein,miR-142-3p could promote the syn- thesis of milk protein and increase the proliferation of mammary epithelial cells by regulating re- lated pathways proteins AKT,mTOR,STAT5 and cyclinD1.
关 键 词:miR-142-3p 催乳素受体 乳腺发育 增殖
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