[1]李姗姗,周良,高琳,等.长链非编码RNA MALAT1促进皮肤鳞癌的发生和发展[J].南方医科大学学报,2018,(04):421.
点击复制

长链非编码RNA MALAT1促进皮肤鳞癌的发生和发展()
分享到:

《南方医科大学学报》[ISSN:1673-4254/CN:44-1627/R]

卷:
期数:
2018年04期
页码:
421
栏目:
出版日期:
2018-04-30

文章信息/Info

Title:
Role of long noncoding RNA MALAT1 promotes the occurrence and progression of cutaneous squamous cell carcinoma
作者:
李姗姗周良高琳王颖慧丁振华
关键词:
LncRNAMALAT1皮肤鳞癌上皮间质转化
Keywords:
long noncoding RNA MALAT1 cutaneous squamous cell carcinoma epithelial-mesenchymal transition
摘要:
目的探索长链非编码RNA MALAT1在皮肤鳞癌发生发展中的作用,为皮肤鳞癌的临床治疗提供基础理论依据。方法 收集55例皮肤鳞癌样本和10例正常皮肤组织样本,采用qRT-PCR与原位杂交方法检测MALAT1在皮肤鳞癌组织和正常组织 中的表达情况。在皮肤鳞癌细胞株A431中,采用siRNAs(siNC, siMALAT1-1, siMALAT1-2)和Lipofectamine2000进行细胞转 染来敲减基因,采用Transwell实验,细胞划痕实验,CCK增殖实验检测皮肤鳞癌细胞的迁移侵袭能力,运动能力和增殖能力。 采用qRT-PCR方法检测A431中MALAT1与上皮间质转化(EMT)样转化相关因子(E-cadherin, Vimentin, β-catenin)的变化;明 确其关系。结果相比正常组织,皮肤鳞癌组织的不同分化水平上(高分化,中分化,低分化),MALAT1 的表达率均升高(P< 0.001)。在皮肤鳞癌细胞A431 中,转染MALAT1 siRNAs 下调其表达后,与对照相比,其增殖能力(P<0.001),迁移能力(P< 0.01),侵袭能力(P<0.01),细胞划痕运动能力均下降(P<0.01)。且EMT相关因子中上皮表型标志物E-cadherin,β-catenin的表 达升高(P<0.01),间质表型分子vimentin 表达降低(P<0.01)。结论长链非编码RNA MALAT1在皮肤鳞癌的发生发展中起促 进作用,可以为皮肤鳞癌的临床治疗提供基础理论依据。
Abstract:
Objective To investigate the role of long noncoding RNA MALAT1 in the occurrence and progression of cutaneous squamous cell carcinoma (CSCC). Methods Fifty-five tissue samples of CSCC and 10 normal epidermal tissues were collected for examination of the expression of MALAT1 using q-PCR and in situ hybridization. Human CSCC A431 cells were transfected with small interfering RNAs (siNC, siMALAT1-1, and siMALAT1-2) using Lipofectamine2000 to knock down MALAT1 gene, and the changes in the cell migration, invasion, mobility and proliferation were analyzed using Transwell assay, wound healing assay, and CCK-8 assay; the changes in the expressions of the related factors of epithelial-mesenchymal transition (EMT), including E-cadherin, vimentin, and β-catenin, were detected using qRT-PCR. Results Compared with normal tissues, CSCC tissues of different grades of differentiation all showed significantly increased expression of MALAT1 (P< 0.001). In A431 cells, MALAT1 knockdown with siRNAs resulted in significantly lowered cell proliferation (P<0.001), migration (P<0.01), invasion (P<0.01), and mobility (P<0.01). Knocking down MALAT1 gene also caused significantly increased expressions of E-cadherin and β-catenin (P<0.01) and lowered the expression of vimentin (P<0.01) in A431 cells. Conclusion The long noncoding RNA MALAT1 promotes the occurrence and progression of CSCC and can potentially serve as a therapeutic target in treatment of CSCC.

相似文献/References:

[1]谢林英,胡志燕,王晓燕,等.长非编码MALAT1基因在人鼻咽癌细胞株的表达及生物学意义[J].南方医科大学学报,2013,(05):692.
[2]韩跃峰,陈德尚,李慧,等.长链非编码RNA MALAT-1基因的敲除抑制人喉鳞状细胞癌Hep-2细胞的增殖和迁移[J].南方医科大学学报,2018,(08):923.

更新日期/Last Update: 1900-01-01