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1.
Eur Rev Med Pharmacol Sci ; 24(13): 7294-7302, 2020 07.
Artículo en Inglés | MEDLINE | ID: mdl-32706067

RESUMEN

OBJECTIVE: Colorectal cancer (CRC) is the fourth leading cause of death worldwide and there is a need for more specific therapeutic targets and biomarkers for the disease. Transforming growth factor ß1-induced transcript 1 (TGFΒ1I1) was reported to be downregulated in CRC tissues; however, the precise roles of TGFΒ1I1 in CRC remain unclear. PATIENTS AND METHODS: The expression of TGFΒ1I1 in CRC cell lines and tissues was assessed by quantitative Polymerase Chain Reaction (qPCR). TGFΒ1I1 was overexpressed in SW620 and RKO cells. Cell viability was analyzed by a CCK-8 assay. The proportion of apoptotic cells was analyzed by flow cytometry. The EdU cell proliferation assay of SW620 and RKO cells after transfection was performed via flow cytometry. The migration potency of SW620 and RKO cells was analyzed using a cell migration assay. A wound healing assay was performed to assess the migration potency of SW620 and RKO cells. The invasion potency of SW620 and RKO cells after TGFΒ1I1 overexpression was analyzed. The protein levels of VEGF, TGF-ß, MMP9, p-Smad2/3, N-cadherin, and E-cadherin were analyzed by Western blot. RESULTS: Decreased expression of TGFΒ1I1 was found in CRC tissues and cell lines. Overexpression of TGFΒ1I1 inhibited the proliferation and induced the apoptosis of CRC cells. The overexpression of TGFΒ1I1 inhibited the migration and invasion of CRC cells. We also found that the overexpression of TGFΒ1I1 in CRC cells inhibited the TGF-ß pathway and epithelial-mesenchymal transition (EMT) progress. CONCLUSIONS: TGFΒ1I1 suppressed cell migration and invasion in CRC by inhibiting the TGF-ß pathway and EMT progress.


Asunto(s)
Movimiento Celular , Neoplasias Colorrectales/metabolismo , Transición Epitelial-Mesenquimal , Péptidos y Proteínas de Señalización Intracelular/metabolismo , Proteínas con Dominio LIM/metabolismo , Apoptosis , Proliferación Celular , Neoplasias Colorrectales/genética , Neoplasias Colorrectales/patología , Regulación Neoplásica de la Expresión Génica , Células HCT116 , Células HT29 , Humanos , Péptidos y Proteínas de Señalización Intracelular/genética , Proteínas con Dominio LIM/genética , Invasividad Neoplásica , Transducción de Señal
2.
Eur Rev Med Pharmacol Sci ; 22(17): 5525-5530, 2018 09.
Artículo en Inglés | MEDLINE | ID: mdl-30229824

RESUMEN

OBJECTIVE: MicroRNAs (miRNAs) play critical roles in regulating tumor development and progression. The aim of the study is to investigate the clinical significance of miR-1294 expression in gastric cancer (GC). PATIENTS AND METHODS: The expression of miR-1294 in 82 cases of GC tissues and adjacent normal tissues was determined using quantitative Real Time-PCR (qRT-PCR) analyses. Survival plot was calculated using the Kaplan-Meier methods and log-rank test from the date of operation to the time of death or last follow-up date. The association between miR-1294 expression and clinical categorical data was analyzed using the chi-squared test. Moreover, Univariate and multivariate Cox analysis were performed to assess the risk factors of GC prognosis. RESULTS: We showed that miR-1294 expression was significantly downregulated in GC tissues compared to adjacent normal tissues. The low expression of miR-1294 in patients with GC was correlated with clinicopathological parameters including larger tumor size, lymph node metastasis, and distant metastasis. Kaplan-Meier survival analysis showed that GC patients with lower miR-1294 expression exhibited a shorter disease-free survival (DFS) and overall survival (OS) time compared to those patients with higher miR-1294 expression. Multivariate Cox analysis showed that lower miR-1294 expression, tumor size, lymph node metastasis, and distant metastasis were identified as independent risk factors of GC prognosis. CONCLUSIONS: Our results provided evidence that miR-1294 expression was significantly downregulated in GC and may serve as a predictor of GC prognosis.


Asunto(s)
Regulación hacia Abajo/fisiología , MicroARNs/biosíntesis , Neoplasias Gástricas/diagnóstico , Neoplasias Gástricas/metabolismo , Adulto , Anciano , Anciano de 80 o más Años , Biomarcadores de Tumor/biosíntesis , Biomarcadores de Tumor/genética , Línea Celular Tumoral , Supervivencia sin Enfermedad , Femenino , Humanos , Masculino , MicroARNs/genética , Persona de Mediana Edad , Pronóstico , Neoplasias Gástricas/genética
3.
Am J Obstet Gynecol ; 142(1): 36-9, 1982 Jan 01.
Artículo en Inglés | MEDLINE | ID: mdl-7055169

RESUMEN

The effect of laminaria-induced cervical dilatation of plasma levels of the prostaglandin metabolite 13, 14-dihydro- 15-keto prostaglandin (PGFM) was evaluated in women undergoing elective first-trimester pregnancy termination. Seventy-one women were randomly assigned to either a treatment (n = 45) or control (n = 26) group. Cervical dilatation measured at the time of insertion of the laminaria was 3.0 +/- 0.1 mm compared to 10.2 +/- 0.2 mm at the time of removal of the laminaria 14 to 16 hours later (p less than 0.001). Peripheral levels of PGFM rose from 28.3 +/- 2.4 pg/ml (mean +/- SEM) to 43.0 +/0 2.6 pg/ml at the time of removal of the laminaria (p less than 0.001). Peripheral concentrations of PGFM in controls remained unchanged. Peripheral concentrations of PGFM did not correlate with the patient's symptoms. Although the hydrophilic property of laminaria is considered to be the principal mechanism promoting cervical dilatation, laminaria may alter the elaboration, release, or degradation of uterine prostaglandin F2 alpha. Thus, biochemical as well as mechanical factors may enhance cervical dilatation in laminaria-treated women.


Asunto(s)
Aborto Inducido , Dinoprost/análogos & derivados , Laminaria , Prostaglandinas F/sangre , Algas Marinas , Adulto , Cuello del Útero/microbiología , Dilatación/métodos , Femenino , Humanos , Embarazo , Primer Trimestre del Embarazo
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