摘要
目的探讨微小RNA-646(miR-646)靶向抑制组蛋白去乙酰化酶2(HDAC2)的表达对T47D和MCF-7乳腺癌细胞增殖和凋亡的影响。方法T47D细胞和MCF-7细胞均分别转染miR-646 negative和miR-646 mimics后命名为T47D-NC组、T47D-miR646组、MCF-7-NC组和MCF-7-miR646组。以细胞计数试剂盒-8实验和集落形成实验观察乳腺癌细胞系增殖活性(OD值)和集落数,以Transwell法检测细胞侵袭能力,以定量逆转录聚合酶链反应检测HDAC2 mRNA表达水平。结果转染96 h时,T47D-NC组、T47D-miR646组、MCF-7-NC组和MCF-7-miR646组OD值分别为0.71±0.08,0.36±0.05,0.80±0.11和0.40±0.08。这4组集落数分别为(203±21),(86±14),(234±19)和(76±11)个。这4组细胞侵袭的数量分别为(56±8),(143±11),(48±9)和(152±13)个。这4组HDAC2 mRNA相对表达水平分别为2.46±0.24,0.94±0.10,2.61±0.31和0.95±0.08。T47D-NC组与T47D-miR646组比较,或MCF-7-NC组与MCF-7-miR646组比较,上述指标差异均有统计学意义(均P<0.05)。结论miR-646作为肿瘤抑制性微小RNA发挥作用,对HDAC2调控可能是其重要作用机制。
Objective To investigate the effect of microRNA-646(miR-646)targeting histone deacetylase 2(HDAC2)on proliferation and apoptosis of T47D and MCF-7 breast cancer cells.Methods T47D cells and MCF-7 cells were respectively transfected with miR-646negative and miR-646 mimics and named as T47D-NC group,T47D-miR646 group,MCF-7-NC group and MCF-7-miR646 group.The proliferative activity(OD value)and colony number of breast cancer cell lines was observed by cell counting kit-8 and colony forming assay.The expression level of HDAC2 mRNA was detected by quantitative reverse transcription polymerase chain reaction(RT-PCR),and the invasive ability of cells was detected by Transwell.Results At 96 h after transfection,the OD values of T47D-NC group,T47D-miR646 group,MCF-7-NC group and MCF-7-miR646 group were 0.71±0.08,0.36±0.05,0.80±0.11 and 0.40±0.08,respectively.The number of colonies in these four groups was 203±21,86±14,234±19 and76±11,respectively.The number of invasive cell in those four groups were 56±8,143±11,48±9 and 152±13,respectively.The relative expression levels of HDAC2 mRNA in these four groups were 2.46±0.24 and 0.94±0.10,2.61±0.31 and 0.95±0.08,respectively.The differences in the above indicators between T47D-NC group and T47D-miR646 group,or between MCF-7-NC group and MCF-7-miR646 group were statistically significant(all P<0.05).Conclusion miR-646 plays a role as a tumor suppressor microRNA,and its regulation of HDAC2 may be an important mechanism.
作者
顾丽
张彩虹
杨丽
陈鹏
GU Li;ZHANG Cai-hong;YANG Li;CHEN Peng(Department of Pathogenic Biology,Baotou Medical College,Inner Mongolia University of Science and Technology,Baotou 014060,Inner Mongolia,China;Department of Laboratory,Affiliated Hospital of Inner Mongolia Medical University,Hohhot 010050,Inner Mogolia,China;Department of Laboratory,The First Affiliated Hospital of Baotou Medical College,Baotou 014010,Inner Mogolia,China;Department of Nutrition,The First Affiliated Hospital of Baotou Medical College,Baotou 014010,Inner Mogolia,China)
出处
《中国临床药理学杂志》
CAS
CSCD
北大核心
2022年第16期1882-1886,共5页
The Chinese Journal of Clinical Pharmacology
基金
内蒙古自然科学基金资助项目(2015MS0855)。
