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1.
Mol Biol Rep ; 46(2): 2039-2047, 2019 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-30710234

RESUMEN

The effects of epigallocatechin-3-gallate (EGCG) and metformin single treatment have been tested against hepatocellular carcinoma (HCC). This study aimed to assess the combination effects of EGCG and metformin on proliferation and apoptosis of HepG2cells and identified new potential molecular targets. The effect of EGCG and metformin against cell proliferation in HepG2 was determined using MTT assay. Reverse transcription polymerase chain reaction was applied to examine the gene expression of cyclin D1, lncRNA-AF085935, caspase-3, survivin and VEGF. The level of protein expression of glypican-3 was assessed by western blot. In HepG2 cells, EGCG and metformin combination treatment exhibited high significant effect against tumor proliferation. It significantly reduced cyclin D1, lncRNA-AF085935, glypican-3 and promoted apoptosis through increasing caspase3 and decreasing survivin compared to control cells. Moreover, EGCG and metformin treated cells showed decreased expression levels of VEGF. Our study provided new insights of the anticarcinogenic effects of EGCG and metformin on HCC through their effects on glypican-3 and lncRNA-AF085935.


Asunto(s)
Carcinoma Hepatocelular/tratamiento farmacológico , Catequina/análogos & derivados , Metformina/farmacología , Anticarcinógenos/farmacología , Apoptosis/efectos de los fármacos , Carcinoma Hepatocelular/metabolismo , Carcinoma Hepatocelular/patología , Caspasa 3/efectos de los fármacos , Catequina/metabolismo , Catequina/farmacología , Línea Celular Tumoral , Proliferación Celular/efectos de los fármacos , Ciclina D1/efectos de los fármacos , Glipicanos/metabolismo , Células Hep G2/efectos de los fármacos , Humanos , Neoplasias Hepáticas/diagnóstico por imagen , Neoplasias Hepáticas/metabolismo , Neoplasias Hepáticas/patología , Metformina/metabolismo , ARN Largo no Codificante/efectos de los fármacos , Transducción de Señal/efectos de los fármacos , Survivin/efectos de los fármacos , Factor A de Crecimiento Endotelial Vascular/efectos de los fármacos
2.
J Interferon Cytokine Res ; 38(11): 517-525, 2018 11.
Artículo en Inglés | MEDLINE | ID: mdl-30383471

RESUMEN

Helicobacter pylori is a ubiquitous Gram-negative bacterium, that is responsible for gastric mucosal inflammation. It is the most common risk factor for gastric cancer (GC). The current study aimed to investigate the association between interleukin-11 (IL-11) and leukemia inhibitory factor (LIF) levels among H. pylori-infected Egyptian patients with gastritis and GC. One hundred forty-seven patients with gastric lesions were endoscopically biopsied and assessed using rapid urease test and immunohistochemistry. Quantitative real-time polymerase chain reaction was done for the detection of H. pylori load in gastric biopsies and detection of LIF as well as IL-11 relative gene expression. The mean values of H. pylori load, LIF, and IL-11 were significantly elevated in GC patients compared to gastritis group (P < 0.0001). A positive significant correlation was detected between mucosal levels of LIF, IL-11, and H. pylori load in both groups. Both LIF and IL-11 had the same pattern of expression in gastric tissues with different types of gastritis and different types and grades of gastric carcinoma. This report could clarify the molecular events associated with the immune response against H. pylori infection and H. pylori-associated pathology. Therefore, development of immunotherapy strategies against H. pylori-induced cytokines becomes inevitable.


Asunto(s)
Infecciones por Helicobacter/inmunología , Infecciones por Helicobacter/microbiología , Helicobacter pylori/patogenicidad , Interleucina-11/inmunología , Factor Inhibidor de Leucemia/metabolismo , Adulto , Egipto , Femenino , Gastritis/genética , Gastritis/inmunología , Gastritis/microbiología , Infecciones por Helicobacter/genética , Humanos , Interleucina-11/genética , Factor Inhibidor de Leucemia/genética , Masculino , Persona de Mediana Edad , Neoplasias Gástricas/genética , Neoplasias Gástricas/inmunología , Neoplasias Gástricas/microbiología
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