ABSTRACT
@#Objective: To explore the influence of circ_0023642 on the proliferation and metastasis of gastric cancer GMC-803 cells by modulating miR-508-3p/ERBB4 axis. Methods: Cancer tissues and corresponding para-cancer normal tissues from 31 gastric cancer patients, who underwent surgical resection at the Second People's Hospital of Nantong City from May 2015 to March 2018, were collected for this study; meanwhile, gastric cancer cell lines (MGC-803, MKN-45 and MKN-28) were also collected. qPCR was performed to determine the expression levels of circ_0023642 and miR-508-3p in above mentioned tissues and cell lines. WB was applied to measure the expressions of ERBB4, E-cadherin, N-cadherin and Vimentin in MGC-803 cells. CCK-8 assay and Transwell assay were used to evaluate the effects of circ_0023462 and miR-508-3p expression on proliferation, migration and invasion of MGC-803 cells. Dual-luciferase reporter gene was carried out to validate whether miR-508-3p could bind to the 3' UTR of circ_0023642 and ERBB4. Results: Compared with para-cancer tissues or normal gastric mucosal cells, the expression of circ_0023642 was significantly up-regulated in gastric cancer tissues and cells lines, and the expression was highest in MGC-803 cells (P<0.05 or P<0.01). Silencing circ_0023642 dramatically decreased the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of MGC-803 cells (P<0.05 or P<0.01). Both circ_0023642 and ERBB4 could target the binding sites of miR-508-3p. Further experiments confirmed that circ_ 0023642 promoted the proliferation, migration, invasion and EMT of MGC-803 cells by sponging miR-508-3p (P<0.05 or P<0.01). Conclusion: circ_0023642, by competing ERBB4 to bind with miR-508-3p, promotes the proliferation and metastasis of gastric cancer MGC-803 cells, thus could be used as a marker for the clinical diagnosis of gastric cancer.
ABSTRACT
Objective This meta-analysis aimed to investigate the association of leptin levels with pathogenetic risk of CHD and stroke. Materials and methods Studies were identified in the PubMed, Embase, and Springer link database without language restriction. Odds ratios (ORs) and corresponding 95% confidence intervals (95% CIs) were used as effect indexes. The association of leptin levels with pathogenetic risk of CHD and stroke, as well as the risk variation of CHD with each additional one unit of leptin level were examined via meta-analysis. The publication bias was assessed via Egger’s linear regression test. Results Eight nested case-control studies consisting of 1,980 patients and 11,567 controls were included for current meta-analysis. ORs (95% CIs) of association of leptin levels with CHD and stroke was 1.90 (1.06, 3.43), and 2.14 (1.48, 3.08), respectively. In addition, significant result was obtained regarding the risk variation of CHD with each additional one unit of leptin level (OR =1.04, 95% CI =1.00‐1.08, P=0.044). There was no significant publication bias as suggested by Egger test outcomes. Conclusion There was a significant association of leptin with pathogenetic risk of CHD and stroke, and raised leptin levels could significantly increase the pathogenetic risk of CHD. .
Objetivo O objetivo desta metanálise foi investigar a associação entre os níveis de leptina e o risco patogenético de doença arterial coronariana e acidente vascular cerebral. Materiais e métodos Foram identificados estudos nas bases de dados PubMed, Embase e Springer Link sem restrição quanto à língua. A razão de chances (OR) e os intervalos de confiança de 95% correspondentes (95% CI) foram usados como índices de efeitos. A associação entre os níveis de leptina e o risco patogenético de doença arterial coronariana e acidente vascular cerebral com cada unidade adicional na concentração de leptina foi analisada por meio de metanálise. O viés da publicação foi avaliado por meio do teste de regressão linear de Egger. Resultados Oito estudos com caso controle aninhado envolvendo 1.980 pacientes e 11.567 controles foram incluídos na metanálise. As ORs (95% CIs) da associação entre as concentrações de leptina e a doença arterial coronariana e o acidente vascular cerebral foram de 1,90 (1,06; 3,43) e 2,14 (1,48; 3,08), respectivamente. Além disso, foram obtidos resultados significativos com a variação de risco para a doença arterial coronariana a cada unidade adicional na concentração de leptina (OR =1,04; 95% CI =1,00‐1,08; P=0,044). Não houve viés de publicação significativo sugerido pelos desfechos no teste de Egger. Conclusão Há associação significativa entre a leptina e o risco patogenético de doença arterial coronariana e acidente vascular cerebral, e concentrações aumentadas de leptina podem elevar significativamente o risco patogenético de doença arterial coronariana. .