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1.
Clin Transl Oncol ; 19(7): 898-906, 2017 Jul.
Article de Anglais | MEDLINE | ID: mdl-28181176

RÉSUMÉ

BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is a common malignant disease worldwide, especially in China. We aimed to determine the level of autoantibodies against L1CAM in patients with ESCC. METHODS: Levels of circulating autoantibodies against L1CAM antigens were determined by an enzyme-linked immunosorbent assay in cohort 1 (191 patients with ESCC and 94 normal controls) and validated in cohort 2 (47 patients with ESCC and 47 normal controls). Receiver-operating characteristics were employed to calculate diagnostic accuracy. Cumulative survival time was calculated by the Kaplan-Meier method and analyzed by the log-rank test. RESULTS: In cohorts 1 and 2, levels of autoantibodies against L1CAM were all significantly higher in sera of patients with ESCC compared to normal controls (P < 0.05). Detection of autoantibodies against L1CAM provided a sensitivity of 26.2%, a specificity of 90.4%, and an area under the curve (AUC) of 0.603 (95% CI 0.535-0.672) in diagnosing ESCC in cohort 1, and a sensitivity of 27.7%, a specificity of 91.5%, and an AUC of 0.628 (95% CI 0.516-0.741). Similar results were observed in the diagnosis of early stage ESCC (25.2% sensitivity, 90.4% specificity, and an AUC of 0.611 (95% CI 0.533-0.689) in cohort 1, and 33.3% sensitivity, 91.5% specificity, and an AUC of 0.636 (95% CI 0.439-0.832) in cohort 2). Moreover, positive rates of autoantibodies against L1CAM had no statistical correlation with clinical outcome of ESCC (P > 0.05). CONCLUSIONS: Our results suggest that circulating autoantibodies against L1CAM is a potential biomarker for the early detection of ESCC.


Sujet(s)
Autoanticorps/sang , Marqueurs biologiques tumoraux/sang , Carcinome épidermoïde/sang , Tumeurs de l'oesophage/sang , Molécule d'adhérence cellulaire neurale L-1/immunologie , Adulte , Sujet âgé , Sujet âgé de 80 ans ou plus , Carcinome épidermoïde/immunologie , Carcinome épidermoïde/secondaire , Carcinome épidermoïde/thérapie , Études cas-témoins , Association thérapeutique , Tumeurs de l'oesophage/immunologie , Tumeurs de l'oesophage/anatomopathologie , Tumeurs de l'oesophage/thérapie , Femelle , Études de suivi , Humains , Métastase lymphatique , Mâle , Adulte d'âge moyen , Invasion tumorale , Pronostic , Courbe ROC , Taux de survie
2.
Genet Mol Res ; 12(2): 1012-21, 2013 Apr 02.
Article de Anglais | MEDLINE | ID: mdl-23613247

RÉSUMÉ

We examined microRNA-181b (miRNA) expression in prostate cancer tissues and its effect on the prostate cancer cell line PC-3. Tissues from 27 cases of prostate cancer and 30 samples of normal human prostate were collected by surgical removal. Total miRNA was extracted, and the relative expression of miR-181b was quantified using RT-PCR. miR-181b ASO was transfected into prostate cancer PC-3 cells. miR-181b expression in transfected and non-transfected cells was measured using RT-PCR. Changes in cell apoptosis were measured using flow cytometry. MTT and cell growth curve methods were used to assess the influence of miR-181b expression on cell proliferation. The changes in cell invasive ability in vitro were detected using the Transwell chamber method. miR-181b was up-regulated in the prostate cancer tissues compared with the normal prostate samples. It was down-regulated after miR-181b ASO transfection into the prostate cancer PC-3 cells. Down-regulation of miR-181b in the PC-3 cell induced apoptosis, inhibited proliferation, and depressed invasion of PC-3 cells in vitro. As miR-181b is over-expressed in prostate cancer, its down-regulation could have potential as gene therapy for prostate cancer by inducing apoptosis, inhibiting proliferation and depressing invasion by cancer cells.


Sujet(s)
Régulation de l'expression des gènes tumoraux , microARN/génétique , microARN/métabolisme , Tumeurs de la prostate/génétique , Tumeurs de la prostate/métabolisme , Apoptose/génétique , Lignée cellulaire tumorale , Mouvement cellulaire/génétique , Prolifération cellulaire , Expression des gènes , Humains , Mâle , Transfection
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