中国临床医学
中國臨床醫學
중국림상의학
Chinese Journal of Clinical Medicine
2015年
5期
582-585
,共4页
沈纳%白广平%高天乐%黄新生%李俊
瀋納%白廣平%高天樂%黃新生%李俊
침납%백엄평%고천악%황신생%리준
喉鳞癌%miRNA-519d%STAT3%增殖%凋亡
喉鱗癌%miRNA-519d%STAT3%增殖%凋亡
후린암%miRNA-519d%STAT3%증식%조망
Laryngeal squamous cell carcinoma%miRNA-519d%Signal transducer and activator of transcription 3%Proliferation%Apoptosis
目的:研究miR‐519d对喉鳞癌细胞增殖及凋亡的调控作用。方法:采用RT‐PCR、Western印迹等技术检测人喉癌上皮细胞株Hep‐2及人支气管上皮细胞(human bronchial epithelium cell ,HBE)中信号转导和转录激活子3(signal transducer and activator of transcription 3,STAT3)以及miR‐519d的表达情况;通过质粒转染上调Hep‐2细胞株中miR‐519d的表达后,采用细胞增殖及凋亡检测技术观察转染细胞与对照细胞的增殖及凋亡情况。结果:STAT3 mRNA在 Hep‐2中的表达明显高于其在HBE细胞中的表达(P<0.05),而miR‐519d在 Hep‐2中的表达明显低于其在 HBE中的表达(P<0.05)。STAT3在转染miR‐519d后的 Hep‐2细胞中的表达明显下降(P<0.05)。转染后继续培养0~7 d ,转染后 Hep‐2细胞的增殖率明显低于未转染细胞(P<0.05)。转染后继续培养24 h ,转染miR‐519d的细胞凋亡率为(2.80±0.15)%,对照细胞的凋亡率为(0.92±0.09)%(P=0.0004)。转染后继续培养72 h ,转染miR‐519d的细胞凋亡率为(23.06±3.52)%,对照细胞的凋亡率为(23.26±2.56)%(P=0.9655)。结论:STAT3在 Hep‐2细胞中高表达,而相关的miR‐519d呈低表达,通过上调miR‐519d可以抑制STAT3的表达从而抑制肿瘤细胞的增殖,促进肿瘤细胞的凋亡。
目的:研究miR‐519d對喉鱗癌細胞增殖及凋亡的調控作用。方法:採用RT‐PCR、Western印跡等技術檢測人喉癌上皮細胞株Hep‐2及人支氣管上皮細胞(human bronchial epithelium cell ,HBE)中信號轉導和轉錄激活子3(signal transducer and activator of transcription 3,STAT3)以及miR‐519d的錶達情況;通過質粒轉染上調Hep‐2細胞株中miR‐519d的錶達後,採用細胞增殖及凋亡檢測技術觀察轉染細胞與對照細胞的增殖及凋亡情況。結果:STAT3 mRNA在 Hep‐2中的錶達明顯高于其在HBE細胞中的錶達(P<0.05),而miR‐519d在 Hep‐2中的錶達明顯低于其在 HBE中的錶達(P<0.05)。STAT3在轉染miR‐519d後的 Hep‐2細胞中的錶達明顯下降(P<0.05)。轉染後繼續培養0~7 d ,轉染後 Hep‐2細胞的增殖率明顯低于未轉染細胞(P<0.05)。轉染後繼續培養24 h ,轉染miR‐519d的細胞凋亡率為(2.80±0.15)%,對照細胞的凋亡率為(0.92±0.09)%(P=0.0004)。轉染後繼續培養72 h ,轉染miR‐519d的細胞凋亡率為(23.06±3.52)%,對照細胞的凋亡率為(23.26±2.56)%(P=0.9655)。結論:STAT3在 Hep‐2細胞中高錶達,而相關的miR‐519d呈低錶達,通過上調miR‐519d可以抑製STAT3的錶達從而抑製腫瘤細胞的增殖,促進腫瘤細胞的凋亡。
목적:연구miR‐519d대후린암세포증식급조망적조공작용。방법:채용RT‐PCR、Western인적등기술검측인후암상피세포주Hep‐2급인지기관상피세포(human bronchial epithelium cell ,HBE)중신호전도화전록격활자3(signal transducer and activator of transcription 3,STAT3)이급miR‐519d적표체정황;통과질립전염상조Hep‐2세포주중miR‐519d적표체후,채용세포증식급조망검측기술관찰전염세포여대조세포적증식급조망정황。결과:STAT3 mRNA재 Hep‐2중적표체명현고우기재HBE세포중적표체(P<0.05),이miR‐519d재 Hep‐2중적표체명현저우기재 HBE중적표체(P<0.05)。STAT3재전염miR‐519d후적 Hep‐2세포중적표체명현하강(P<0.05)。전염후계속배양0~7 d ,전염후 Hep‐2세포적증식솔명현저우미전염세포(P<0.05)。전염후계속배양24 h ,전염miR‐519d적세포조망솔위(2.80±0.15)%,대조세포적조망솔위(0.92±0.09)%(P=0.0004)。전염후계속배양72 h ,전염miR‐519d적세포조망솔위(23.06±3.52)%,대조세포적조망솔위(23.26±2.56)%(P=0.9655)。결론:STAT3재 Hep‐2세포중고표체,이상관적miR‐519d정저표체,통과상조miR‐519d가이억제STAT3적표체종이억제종류세포적증식,촉진종류세포적조망。
Objective:To investigate the effect of up‐regulating miR‐519d on proliferation and apoptosis of laryngeal squamous cell carcinoma .Methods:The expression of signal transducer and activator of transcription 3 (STAT3) and miR‐519d in human laryngeal carcinoma epithelium cell line Hep‐2 and human bronchial epithelium cell (HBE ) were detected by real‐time fluorescent quantitative polymerase chain reaction (RT‐PCR) and Western blotting .After up‐regulating miR‐519d expression in Hep‐2 cell line by plasmid transfection technique ,the proliferation and apoptosis of transfected cells and control cells was detected by proliferation and apoptosis assays .Results:STAT3 mRNA expression in Hep‐2 cells was significantly higher than that in HBE cells (P<0 .05) .However ,miR‐519d expression in Hep‐2 cells was significantly lower than that in HBE cells (P<0 .05) .The STAT3 mRNA expression in the transfected Hep‐2 cells decreased significantly .During 0 and 7 day of post‐transfection culture ,proliferation rate of transfected Hep‐2 cells was significantly lower than that of untransfected cells (P<0 .05) .After 24 h culture ,the apoptosis rate of miR‐519d transfected cells was (2 .8 ± 0 .15)% ,while that of control cells was (0 .92 ± 0 .09)% (P=0 .000 4) .After 72 h culture ,the apoptosis rate of miR‐519d transfected cells was (23 .06 ± 3 .52)% , while that of control cells was (23 .26 ± 2 .56)% (P=0 .965 5) .Conclusions:STAT3 shows high expression in Hep‐2 cell , while the related miR‐519d shows low expression .By up‐regulating miR‐519d ,STAT3 expression could be suppressed ,so as to suppress the proliferation of tumor cells and promote the apoptosis of tumor cells .