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1.
Chinese Journal of School Health ; (12): 1894-1897, 2023.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-1004914

RESUMO

Objective@#To understand the prevalence and associated factors of functional constipation(FC) among primary and middle school students in Shaanxi Province, in order to provide a basis for preventing FC in students.@*Methods@#A stratified cluster random sampling method was used to conduct a questionnaire survey on 9 133 primary and middle school students aged 10-18 in eight primary and secondary schools in Shaanxi Province from March to September,2017. Chi square test and multivariate Logistic regression were used to analyze the associated factors of FC among primary and middle school students in Shaanxi Province.@*Results@#There were a total of 364 students meeting the FC Rome IV diagnostic criteria, with a prevalence rate of 3.99%. Among them, there were 155 male students with a prevalence rate of 3.43%, and 209 female students with a prevalence rate of 4.53%. Univariate analysis showed that gender, breastfeeding, separation from parents, long term school meals, types of staple foods, breakfast frequency, cold foods eating frequency, spicy foods eating frequency, fried food eating frequency, pickled food eating frequency, desserts eating frequency, vegetables eating frequency were related to FC, and the differences were statistically significant ( χ 2=7.30,18.75, 20.89,35.54,22.43,16.05,21.31,13.97,10.33,23.96,16.25,17.74, P <0.05). Multivariate Logistic regression analysis showed that female, non breastfeeding, separation from parents, long term school meals, low consumption of staple food/staple food dominated by rice, and never eating vegetables were positively correlated with FC( OR =1.37,1.96,1.52,2.07,1.76,1.58,2.31, P < 0.05 ).@*Conclusions@#The prevalence of functional constipation is higher in primary and middle school students. Attention should be paid to factors related to students dietary habits and food classification to prevent the occurrence of FC in primary and middle school students.

3.
Mol Oncol ; 12(11): 1949-1964, 2018 11.
Artigo em Inglês | MEDLINE | ID: mdl-30171794

RESUMO

miR-372/373, a cluster of stem cell-specific microRNAs transactivated by the Wnt pathway, has been reported to be dysregulated in various cancers, particularly colorectal cancer (CRC); however, the unique role of these microRNAs in cancer remains to be discovered. In the present study, we characterized the upregulation in expression of miR-372/373 in CRC tissues from The Cancer Genome Atlas data, and then showed that overexpression of miR-372/373 enhanced the stemness of CRC cells by enriching the CD26/CD24-positive cell population and promoting self-renewal, chemotherapy resistance and the invasive potential of CRC cells. To clarify the mechanism underlying microRNA-induced stemness, we profiled 45 cell signaling pathways in CRC cells overexpressing miR-372/373 and found that stemness-related pathways, such as Nanog and Hedgehog, were upregulated. Instead, differentiation-related pathways, such as NFκB, MAPK/Erk and VDR, were markedly repressed by miR-372/373. Numerous new targets of miR-372/373 were identified, including SPOP, VDR and SETD7, all of which are factors important for cell differentiation. Furthermore, in contrast to the increase in miR-372/373 expression in CRC tissues, the expression levels of SPOP and VDR mRNA were significantly downregulated in these tissues, indicative of the poor differentiation status of CRC. Taken together, our findings suggest that miR-372/373 enhance CRC cell stemness by repressing the expression of differentiation genes. These results provide new insights for understanding the function and mechanisms of stem cell-specific microRNAs in the development of metastasis and drug resistance in CRC.


Assuntos
Neoplasias Colorretais/metabolismo , Sistema de Sinalização das MAP Quinases , MicroRNAs/metabolismo , Células-Tronco Neoplásicas/metabolismo , RNA Neoplásico/metabolismo , Animais , Células CACO-2 , Neoplasias Colorretais/genética , Neoplasias Colorretais/patologia , Feminino , Regulação Neoplásica da Expressão Gênica , Células HCT116 , Humanos , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , MicroRNAs/genética , Proteínas de Neoplasias/genética , Proteínas de Neoplasias/metabolismo , Células-Tronco Neoplásicas/patologia , RNA Neoplásico/genética
4.
Oncotarget ; 7(27): 42513-42526, 2016 Jul 05.
Artigo em Inglês | MEDLINE | ID: mdl-27285761

RESUMO

A hallmark of aberrant activation of the Wnt/ß-catenin signaling pathway has been observed in most colorectal cancers (CRC), but little is known about the role of non-coding RNAs regulated by this pathway. Here, we found that miR-150 was the most significantly upregulated microRNA responsive to elevated of Wnt/ß-catenin signaling activity in both HCT116 and HEK293T cells. Mechanistically, the ß-catenin/LEF1 complex binds to the conserved TCF/LEF1-binding element in the miR-150 promoter and thereby transactivates its expression. Enforced expression of miR-150 in HCT116 cell line transformed cells into a spindle shape with higher migration and invasion activity. miR-150 markedly suppressed the CREB signaling pathway by targeting its core transcription factors CREB1 and EP300. Knockdown of CREB1 or EP300 and knockout of CREB1 by CRISPR/Cas9 phenocopied the epithelial-mesenchymal transition (EMT) observed in HCT116 cells in response to miR-150 overexpression. In summary, our data indicate that miR-150 is a novel Wnt effector that may significantly enhance EMT of CRC cells by targeting the CREB signaling pathway.


Assuntos
Transição Epitelial-Mesenquimal , MicroRNAs/metabolismo , Via de Sinalização Wnt , beta Catenina/metabolismo , Animais , Movimento Celular , Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo , Progressão da Doença , Proteína p300 Associada a E1A/metabolismo , Regulação Neoplásica da Expressão Gênica , Células HCT116 , Células HEK293 , Humanos , Fator 1 de Ligação ao Facilitador Linfoide/metabolismo , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , Ativação Transcricional , Transfecção
5.
Mol Cancer Ther ; 11(5): 1155-65, 2012 May.
Artigo em Inglês | MEDLINE | ID: mdl-22389469

RESUMO

The transcription factor c-Myc is important in cell fate decisions and is frequently overexpressed in cancer cells, making it an attractive therapeutic target. Natural compounds are among the current strategies aimed at targeting c-Myc, but their modes of action still need to be characterized. To explore the mechanisms underlying the anticancer activity of a natural diterpenoid, oridonin, we conducted miRNA expression profiling and statistical analyses that strongly suggested that c-Myc was a potential molecular target of oridonin. Furthermore, experimental data showed that oridonin significantly reduced c-Myc protein levels in vitro and in vivo and that this reduction was mediated by the ubiquitin-proteasome system. Fbw7, a component of the ubiquitin-proteasome system and an E3 ubiquitin ligase of c-Myc, was upregulated rapidly in K562 cells and other leukemia and lymphoma cells, resulting in the rapid turnover of c-Myc. In cell lines harboring mutations in the WD domain of Fbw7, the degradation of c-Myc induced by oridonin was attenuated during short-term treatment. GSK-3, an Fbw7 priming kinase, was also activated by oridonin, along with an increase in T58-phosphorylated c-Myc. Furthermore, the knockdown of Fbw7 or the forced expression of stable c-Myc resulted in reduced sensitization to oridonin-induced apoptosis. Our observations help to clarify the anticancer mechanisms of oridonin and shed light on the application of this natural compound as an Fbw7-c-Myc pathway targeting agent in cancer treatment.


Assuntos
Antineoplásicos Fitogênicos/farmacologia , Apoptose/efeitos dos fármacos , Proteínas de Ciclo Celular/metabolismo , Diterpenos do Tipo Caurano/farmacologia , Proteínas F-Box/metabolismo , Complexo de Endopeptidases do Proteassoma/metabolismo , Proteínas Proto-Oncogênicas c-myc/metabolismo , Ubiquitina-Proteína Ligases/metabolismo , Animais , Proliferação de Células/efeitos dos fármacos , Ativação Enzimática/efeitos dos fármacos , Proteína 7 com Repetições F-Box-WD , Perfilação da Expressão Gênica , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Quinase 3 da Glicogênio Sintase/metabolismo , Células HL-60 , Humanos , Células K562 , Camundongos , Camundongos Endogâmicos NOD , Camundongos SCID , MicroRNAs/genética , Fosforilação/efeitos dos fármacos , Estabilidade Proteica/efeitos dos fármacos , Proteínas Proto-Oncogênicas c-myc/genética , Transdução de Sinais/efeitos dos fármacos , Ubiquitina/metabolismo
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