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Downregulation of miR-486-5p contributes to tumor progression and metastasis by targeting protumorigenic ARHGAP5 in lung cancer

Wang, J ; Tian, X ; Han, R ; Zhang, X ; Wang, X ; Shen, H ; Xue, L ; Liu, Y ; Yan, X ; Shen, J ; Mannoor, K ; Deepak, J ; Donahue, J M ; Stass, S A ; Xing, L ; Jiang, F

Oncogene, 2014-02, Vol.33 (9), p.1181-1189 [Periódico revisado por pares]

England: Nature Publishing Group

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Título:
Downregulation of miR-486-5p contributes to tumor progression and metastasis by targeting protumorigenic ARHGAP5 in lung cancer
Autor: Wang, J ; Tian, X ; Han, R ; Zhang, X ; Wang, X ; Shen, H ; Xue, L ; Liu, Y ; Yan, X ; Shen, J ; Mannoor, K ; Deepak, J ; Donahue, J M ; Stass, S A ; Xing, L ; Jiang, F
Assuntos: 3' Untranslated regions ; 3' Untranslated Regions - genetics ; Cancer ; Carcinogenesis ; Carcinogenesis - genetics ; Carcinogenesis - pathology ; Carcinoma, Non-Small-Cell Lung - genetics ; Carcinoma, Non-Small-Cell Lung - pathology ; Cell adhesion & migration ; Cell Line, Tumor ; Cell migration ; Cell Movement - genetics ; Cell Proliferation ; Chromosome 5 ; Complications and side effects ; Development and progression ; Disease Progression ; Down-Regulation - genetics ; Ectopic expression ; Gene therapy ; GTPase-Activating Proteins - genetics ; Humans ; Kinases ; Lung cancer ; Lung cancer, Non-small cell ; Lung Neoplasms - genetics ; Lung Neoplasms - pathology ; Lymph nodes ; Lymphatic Metastasis - genetics ; Lymphatic Metastasis - pathology ; Metastases ; Metastasis ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; Non-small cell lung carcinoma ; Oncology, Experimental ; Paraffin ; Physiological aspects ; RNA-directed DNA polymerase ; Small cell lung carcinoma ; Therapeutic targets ; Tumor suppressor genes ; Tumorigenesis ; Tumors ; Up-Regulation - genetics
É parte de: Oncogene, 2014-02, Vol.33 (9), p.1181-1189
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
These authors contributed equally to this work.
Descrição: We have previously shown that miR-486-5p is one of the most downregulated micro RNAs in lung cancer. The objective of the study was to investigate the role of miR-486-5p in the progression and metastasis of non-small-cell lung cancer (NSCLC). We evaluated miR-486-5p expression status on 76 frozen and 33 formalin-fixed paraffin-embedded tissues of NSCLC by quantitative reverse transcriptase PCR to determine its clinicopathologic significance. We then performed function analysis of miR-486-5p to determine its potential roles on cancer cell migration and invasion in vitro and metastasis in vivo. We also investigated the target genes of miR-486-5p in lung tumorigenesis. miR-486-5p expression level was significantly lower in lung tumors compared with their corresponding normal tissues (P<0.0001), and associated with stage (P=0.0001) and lymph node metastasis of NSCLC (P=0.0019). Forced expression of miR-486-5p inhibited NSCLC cell migration and invasion in vitro and metastasis in mice by inhibiting cell proliferation. Furthermore, ectopic expression of miR-486-5p in cancer cells reduced ARHGAP5 expression level, whereas miR-486-5p silencing increased its expression. Luciferase assay demonstrated that miR-486-5p could directly bind to the 3'-untranslated region of ARHGAP5. The expression level of miR-486-5p was inversely correlated with that of ARHGAP5 in lung tumor tissues (P=0.0156). Reduced expression of ARHGAP5 considerably inhibited lung cancer cell migration and invasion, resembling that of miR-486-5p overexpression. miR-486-5p may act as a tumor-suppressor contributing to the progression and metastasis of NSCLC by targeting ARHGAP5. miR-486-5p would provide potential diagnostic and therapeutic targets for the disease.
Editor: England: Nature Publishing Group
Idioma: Inglês

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Downregulation of miR-486-5p contributes to tumor progression and metastasis by targeting protumorigenic ARHGAP5 in lung cancer

Wang, J ; Tian, X ; Han, R ; Zhang, X ; Wang, X ; Shen, H ; Xue, L ; Liu, Y ; Yan, X ; Shen, J ; Mannoor, K ; Deepak, J ; Donahue, J M ; Stass, S A ; Xing, L ; Jiang, F

England: Nature Publishing Group

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