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1.
J Surg Res ; 193(2): 718-23, 2015 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-25439221

RESUMEN

BACKGROUND: MicroRNA 138 (miR-138) is recently shown to inhibit tumor growth and block cell cycle arrest of hepatocellular carcinoma (HCC) by targeting cyclin D3 (CCND3). The aim of this study was to investigate the clinical significance of miR-138 and CCND3 in human HCC, which remains unclear. METHODS: Quantitative real-time polymerase chain reaction analysis was performed to detect the expression levels of miR-138 and CCND3 messenger RNA (mRNA) in 180 self-pairs of HCC and noncancerous liver tissues. RESULTS: Compared with noncancerous liver tissues, the expression levels of miR-138 in HCC tissues were significantly downregulated (P < 0.001), whereas the expression levels of CCND3 mRNA in HCC tissues were significantly upregulated (P < 0.001). There was a negative correlation between miR-138 and CCND3 mRNA expression in HCC tissues (r = -0.56, P = 0.02). Additionally, statistical analysis showed that the combined miR 138 downregulation and CCND3 upregulation (miR-138-low-CCND3-high) was significantly associated with the advanced tumor-node-metastasis stage (P = 0.008) and the presence of portal vein invasion (P = 0.008) and lymph node metastasis (P = 0.01). More importantly, a significant trend was identified between the combined expression of miR-138-low-CCND3-high in HCC and worsening clinical prognosis. Multivariate survival analysis further recognized miR-138-low-CCND3-high expression as an independent prognostic factor for patients with HCC. CONCLUSIONS: Our data suggest that the combined expression of miR-138 and its direct target CCND3 may be correlated with significant characteristics of HCC. MiR-138 downregulation and CCND3 upregulation maybe concurrently associated with prognosis in patients with HCC.


Asunto(s)
Carcinoma Hepatocelular/patología , Ciclina D3/metabolismo , Neoplasias Hepáticas/patología , Hígado/patología , MicroARNs/metabolismo , Carcinoma Hepatocelular/metabolismo , Carcinoma Hepatocelular/mortalidad , China/epidemiología , Femenino , Regulación Neoplásica de la Expresión Génica , Humanos , Neoplasias Hepáticas/metabolismo , Neoplasias Hepáticas/mortalidad , Masculino , Persona de Mediana Edad
2.
J Environ Public Health ; 2022: 5833589, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-36159750

RESUMEN

In the context of the new era, the distinctive function of BD (big data) analysis and prediction also introduces a new way of thinking to university IPE (ideological and political education), broadens the domain of university IPE, and enhances the curricular offerings of IPE universities. In order to enhance the intelligence and personalization of the intelligent teaching system, this paper describes in detail the design and implementation processes for each component of the system. It also uses the association mining rule algorithm of data mining. To maintain population diversity, a population initialization method and a neighborhood-based search operator are used, both of which are based on a thorough consideration of the characteristics of complex networks. The neighborhood search strategy enhances the local search capability of the TLBO (Teaching-Learning Based Optimization) algorithm. The optimized TLBO algorithm presented in this paper achieves the highest average modularity value of 0.5238 through testing on real-world data sets. The outcomes demonstrate that the algorithm performs well and is successful in identifying problems in the community.


Asunto(s)
Curriculum , Análisis de Datos , Algoritmos , Humanos , Aprendizaje , Universidades
3.
Mol Med Rep ; 24(5)2021 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-34542163

RESUMEN

Subsequently to the publication of this paper, an interested reader drew to the authors' attention that strikingly similar western blot data were shown in Fig. 2 (to portray the Nagon data in Fig. 2A and the CD133 data in Fig. 2B), and the same data also appeared to have been included in Fig. 4 (to show the p­FOXO3a data). After having examined their original data, the authors have realized that these figures were inadvertently assembled incorrectly. The corrected versions of Figs. 2 and 4, showing the correct data for the CD133 experiment in Fig. 2B and the p­FOXO3a experiment in Fig. 4, are shown opposite. Note that these errors did not significantly affect the results or the conclusions reported in this paper, and all the authors agree to this Corrigendum. Furthermore, the authors apologize to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 9: 1982­1988, 2014; DOI: 10.3892/mmr.2014.2012].

4.
Life Sci ; 244: 117298, 2020 Mar 01.
Artículo en Inglés | MEDLINE | ID: mdl-31953163

RESUMEN

Long non-coding RNA (lncRNA) is emerging as an essential player in cancer progression. However, its biological function and clinical implication in papillary thyroid carcinoma (PTC) remain poorly understood. In the current study, we found that a novel lncRNA, ASMTL antisense RNA 1 (ASMTL-AS1), was significantly downregulated in PTC. And its downregulation was positively linked to larger tumor size, advanced clinical stage and unfavorable outcome. Overexpression of ASMTL-AS1 evidently inhibited PTC cell proliferation and glycolysis, while knockdown of ASMTL-AS1 resulted in the opposite effect. Regarding the mechanism, ASMTL-AS1 was capable of sponging miR-93-3p and miR-660 to elevate FOXO1 expression, leading to repressing glycolysis and tumorigenesis. In turn, FOXO1 could also increase ASMTL-AS1 expression via directly binding to ASMTL-AS1 promoter, which formed a positive feedback regulation loop. Importantly, the regulatory axis of ASMTL-AS1/miR-93-3p/miR-660/FOXO1 was also identified in vivo. Collectively, our data clearly indicate that ASMTL-AS1 functions as a novel tumor suppressor in PTC through regulation of miR-93-3p/miR-660/FOXO1 pathway. Targeting ASMTL-AS1 and its downstream pathway may be an effective therapeutic approach for patients with PTC.


Asunto(s)
Proteína Forkhead Box O1/metabolismo , Regulación Neoplásica de la Expresión Génica , Glucólisis , MicroARNs/genética , ARN Largo no Codificante/genética , Cáncer Papilar Tiroideo/patología , Animales , Apoptosis , Biomarcadores de Tumor/genética , Biomarcadores de Tumor/metabolismo , Estudios de Casos y Controles , Proliferación Celular , Femenino , Estudios de Seguimiento , Proteína Forkhead Box O1/genética , Humanos , Masculino , Metiltransferasas/antagonistas & inhibidores , Ratones , Ratones Desnudos , Persona de Mediana Edad , Pronóstico , ARN sin Sentido/genética , Tasa de Supervivencia , Cáncer Papilar Tiroideo/genética , Cáncer Papilar Tiroideo/metabolismo , Neoplasias de la Tiroides/genética , Neoplasias de la Tiroides/metabolismo , Neoplasias de la Tiroides/patología , Células Tumorales Cultivadas , Ensayos Antitumor por Modelo de Xenoinjerto
5.
Mol Med Rep ; 9(5): 1982-8, 2014 May.
Artículo en Inglés | MEDLINE | ID: mdl-24604613

RESUMEN

Carcinogenesis is predominantly dependent on the cancer stem cells (CSCs) residing or populating within the cancer. We previously demonstrated that the novel synthetic genistein analogue, 7-difluoromethoxyl-5,4'-di-n-octylgenistein (DFOG), induced apoptotic cell death of ovarian and gastric cancer cells. The present study demonstrated that sphere­forming cells (SFCs) derived from the ovarian cancer cell-line SKOV3 possessed ovarian cancer stem-like cell (OCSLC) properties, including self-renewal and high tumorigenicity. DFOG may be effective in inhibiting the self­renewal capacity of SFCs derived from the SKOV3 cell line. DFOG decreased the level of phosphorylated FOXO3a protein in SKOV3 cell­derived SFCs. The inhibition of FOXO3a expression by siRNA significantly attenuated the ability of DFOG to inhibit the self-renewal capacity of SKOV3-derived SFCs. Our results suggested that DFOG has been demonstrated to significantly inhibit the self-renewal capacity of ovarian cancer stem cells (OCSCs) through a mechanism partly dependent on the activation of FOXO3a.


Asunto(s)
Factores de Transcripción Forkhead/genética , Genisteína/análogos & derivados , Células Madre Neoplásicas/efectos de los fármacos , Células Madre Neoplásicas/metabolismo , Neoplasias Ováricas/genética , Animales , Biomarcadores de Tumor/genética , Biomarcadores de Tumor/metabolismo , Línea Celular Tumoral , Transformación Celular Neoplásica/efectos de los fármacos , Transformación Celular Neoplásica/genética , Transformación Celular Neoplásica/metabolismo , Modelos Animales de Enfermedad , Femenino , Proteína Forkhead Box O3 , Factores de Transcripción Forkhead/metabolismo , Técnicas de Inactivación de Genes , Genisteína/farmacología , Xenoinjertos , Humanos , Neoplasias Ováricas/patología , Fosforilación/efectos de los fármacos , Esferoides Celulares , Células Tumorales Cultivadas , Ensayo de Tumor de Célula Madre
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