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作 者:李志强[1] 邹瑞[2] 欧阳可雄[2] 白植宝[3] 艾伟健[1] LI Zhi-qiang;ZOU Rui;OUYANG Ke-xiong;BAI Zhi-bao;AI Wei-jian(Department of Oral and Maxillofacial Surgery, Guangdong Provincial Stomatological Hospital, the Affiliated Stomatological Hospital of Southern Medical University, Guangzhou 510280, China;Key Laboratory of Oral Medicine, Guangzhou Institute of Oral Disease, Stomatology Hospital of Guangzhou Medical University; Guangzhou 510140, China;Department of Stomatology Guangzhou First Peoples′ Hospital, Guangzhou 510180, China)
机构地区:[1]广东省口腔医院.南方医科大学附属口腔医院口腔颌面外科,广东广州510280 [2]广州医科大学附属口腔医院.广州口腔疾病研究所.口腔医学重点实验室,广东广州510140 [3]广州市第一人民医院口腔科,广东广州510180
出 处:《口腔疾病防治》2016年第9期511-514,共4页Journal of Prevention and Treatment for Stomatological Diseases
基 金:广东省医学科研基金(A2014106);广东省科技计划项目(2013B021800196;20120318025)
摘 要:目的研究长链非编码RNA牛磺酸上调基因1(taurine upregulated gene 1,TUG1)在舌鳞状细胞癌及癌旁组织中的表达差异,探讨TUG1在舌鳞状细胞癌中可能的作用机理。方法荧光实时定量PCR法检测19例患者舌鳞状细胞癌组织及其对应的癌旁组织中TUG1的表达差异,利用小干扰RNA(small interfering RNA,si RNA)技术在舌鳞状细胞癌细胞系CAL27中沉默TUG1的表达,并用四甲基偶氮唑盐(methylthiazolyl tetrazolium,MTT)法检测细胞增殖能力变化,荧光实时定量PCR法检测下游相关基因诱导型一氧化氮合酶(inducible nitric oxide synthase,i NOS)基因的表达改变。结果 TUG1在舌鳞状细胞癌组织标本中相对癌旁组织呈高表达状态(P<0.001)。利用si RNA技术沉默TUG1的表达后,舌鳞状细胞癌细胞系CAL27细胞增殖能力显著下降,转染si RNA后24 h、48 h、72 h,细胞增殖抑制率分别为14.16%、16.96%、21.40%。实验组、空白对照组和阴性对照组i NOS基因的相对表达量为1.000±0.034、0.974±0.045、0.729±0.039,沉默TUG1的实验组的i NOS基因表达受到了明显抑制(P=0.002)。结论长链非编码RNA TUG1在舌鳞状细胞癌中可能起到致癌基因的作用,且其可能通过促进i NOS的表达调控舌鳞状细胞癌的生长。Objective To study the expression of LncRNA TUG1 in tongue squamous cell carcinoma (TSCC), and explore its function in the development of TSCC. Methods Fresh samples of TSCC tissues and corresponding adjacent normal tongue tissues were obtained from 19 cases, and the expressions of TUG1were detected by Q?PCR. The expression of TUG1 in CAL27 cell line were down?regulated by siRNA technology, and the cell proliferation ability after transfection was analyzed by MTT assay. The expressions of iNOS gene were rated by Q?PCR. Results Result of Q-PCR revealed the expressions of LncRNA TUG1 were up?regulated in TSCC tissues compared with the adjacent normal tongue tissues (P < 0.001). Cell proliferation ability was inhibited after down?regulation of TUG1 by siRNA technology, and the inhibition rates of 24/48/72 hour were 14.16%. 16.96% and 21.40% respectively. The relative expression of iNOS in blank/control/experimental groups were 1.000 ± 0.034, 0.974 ± 0.045 and 0.729 ± 0.039 respectively, and iNOS was down- regulated significantly in the experimental group (P = 0.002). Conclusion LncRNA TUG1 may have functions as a cancerogenic substance in TSCC via pormoting the expression of iNOS.
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