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miRNA-21调控MACC1蛋白诱导宫颈癌细胞凋亡的研究 被引量:1

Study on the miRNA-21 regulates MACC1 protein induced apoptosis in cervical cancer cells
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摘要 目的探讨miRNA-21对宫颈癌细胞生长和凋亡的影响。方法合成miRNA-21和对照微小RNA(miRNA)并转染到Hela宫颈癌细胞中。使用噻唑基蓝四唑溴化物(MTT)测定半胱天冬酶-3(caspase-3)活性,采用流式细胞术研究miRNA-21对Hela细胞生长和细胞凋亡的影响。合成靶向结肠癌转移相关基因-1(MACC1)的小干扰RNA,并将其与miRNA-21一起转染到Hela细胞中,分别通过免疫蛋白质印迹法和流式细胞术测量MACC1表达和细胞凋亡情况。结果miRNA-21转染到Hela细胞中抑制其生长,促进了其凋亡,同时活化的caspase-3表达水平降低。MACC1表达降低显著增加了miRNA-21诱导的Hela细胞凋亡。结论MACC1可能作为miRNA-21的作用靶点,参与宫颈癌细胞的凋亡行为调控。 Objective To investigate the effects of miRNA-21 on the growth and apoptosis of cervical cancer cells.Methods miRNA-21 and control MicroRNA(miRNA)were synthesized and transfected into Hela cervical cancer cells.The caspase-3 activity was investigated by thiazolyl blue tetrazolium bromide(MTT)assay,and the effect of miRNA-21 on Hela cell growth and apoptosis was studied by flow cytometry.Small interfering RNA of targeting MACC1 was synthesized and transfected into Hela cells together with miRNA-21.MACC1 expression and apoptosis were measured by Western blotting and flow cytometry,respectively.Results miRNA-21 was transfected into Hela cells to inhibit its growth and promote its apoptosis,while the expression level of activated caspase-3 was decreased.The decrease of MACC1 expression significantly increased the apoptosis of Hela cells induced by miRNA-21.Conclusion MACC1 may be a target of miRNA-21 and participate in the regulation of apoptosis in cervical cancer cells.
作者 梁皓 刘帅斌 李虎 胡丽娜 LIANG Hao;LIU Shuaibin;LI Hu;HU Li′na(Department of Obstetrics and Gynecology,the Second Affiliated Hospital of Chongqing Medical University,Chongqing 400010,China)
出处 《现代医药卫生》 2020年第11期1638-1641,共4页 Journal of Modern Medicine & Health
关键词 宫颈癌 MIRNA-21 结肠癌转移相关基因-1 凋亡 Cervical cancer miRNA-21 Metastasis-associated in colon cancer-1 Apoptosis
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  • 1IOIRO MV, FERRACINM, LIU CG, et al. MicroRNA gene expres- sion deregulation in human breast cancer [J]. Cancer Res, 2005,65 (16) : 7065-7070.
  • 2KARP X, AMBROS V. Developmental biology, encountering mi- croRNAs in cell fatesignaling [J]. Science, 2005, 310 (5752) : 1288-1289.
  • 3LAGOS QUINTANA M, RAUHUT R, LENDECKE1 W, et al. Identi- fication of novel genescoding for small expressed RNAs [J]. Sci- ence, 2001,294 (5543) : 853 -858.
  • 4CHEN CZ, L1 L, LODISH HF, et al. MicroRNAs modulate hemato- poietic lineage differentiation ~J]. Science, 2004, 303 (5654) : 83- 86.
  • 5BOUTLA A, DELIDAKIS C, TABLER M. Developmental defects byantisense-mediated inactivation of micro-RNAs 2 and 13 in Dro- sophila and the identification of putative target genes [J]. Nucleic Acids Res,2003,31 (17) :4973-4980.
  • 6LEE YS, KIM HK, CHUNG S, et al. Depletion of human microRNA miR-125b reveals that it is critical for the proliferation ofdifferentiat- ed cells but not for the down-regulation of putative targets during dif- ferentiation [Jl. J Biol Chem, 2005,280(17) :16635-16641.
  • 7VOLINIA S, CALIN GA, LIU CG, et al. A micro-RNA expression signature of humansolid tumors defines cancer gene targets [J].Proc Natl Acad Sci USA, 2006,103 (7) :2257-2261.
  • 8KNAUPER V, WILL H, LOPEZ-TINC, et al. Cellular mechanisms for human procollagenase- 3 (MMP- 13 ) activation. Evidence that MT1-MMP(MMP-14)and gelatinase a (MMP-2) are able to gener- ate activeenzyme [J]. J Biol Chem, 1996,271 (29) : 17124-17131.
  • 9BRAUER PR. MMPs roleincardiovasculardevelopment anddisease [J~. Front Siosei, 2006,11 ( 1 ) : 447-478.
  • 10HAAS J. High dose IVIG in the postpartum period for prevention of exacerbations in MS [J ]. Mult Scler, 2000,6 (Suppl 2):18-20.

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