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Role of long noncoding RNA MALAT1 promotes the occurrence and progression of cutaneous squamous cell carcinoma / 南方医科大学学报
Journal of Southern Medical University ; (12): 421-427, 2018.
Artigo em Chinês | WPRIM | ID: wpr-690452
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the role of long noncoding RNA MALAT1 in the occurrence and progression of cutaneous squamous cell carcinoma (CSCC).</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>The long noncoding RNA MALAT1 promotes the occurrence and progression of CSCC and can potentially serve as a therapeutic target in treatment of CSCC.</p>
Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Journal of Southern Medical University Ano de publicação: 2018 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Journal of Southern Medical University Ano de publicação: 2018 Tipo de documento: Artigo