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This study aimed to observe the differential expression of Annexin-A1 in esophageal squamous cell carcinoma (ESCC) and explored the effect of small interfering ribonucleic acid (RNAi)-Annexin-A1 on the biological behavior of CE81T-0 cells. An immunohistochemical approach was used to detect the expression of Annexin-A1 in 86 pairs of ESCC samples. Quantitative reverse transcription polymerase chain reaction was used to detect the expression of Annexin-A1 in CE81T-0 and CE81T-4 cells, and the expression of Annexin-A1 in CE81T-0 cells was knocked out by RNAi. A methyl-thiazolyltetrazolium assay was used to observe the effect of Annexin-A1 on cell proliferation, and flow cytometry was conducted to analyze its effect on cell cycles and apoptosis. A scratch assay and a Transwell chamber were used to detect changes in cell migration and invasion. From the results, compared with the Annexin-A1 expression rate of 59.3% in para-carcinoma tissues, the expression of Annexin-A1 in cancer was reduced to only 32.6% in ESCC cells. Annexin-A1 was strongly expressed in highly differentiated ESCC cells without lymphatic metastasis and highly expressed in the CE81T-0 cell group with low metastasis. Annexin-A1 gene silencing promoted cell proliferation and inhibited apoptosis, blocked cells in the S-phase, and increased cell migration, leading to an increase in the number of invaded cells. Above all, Annexin-A1 could reflect the differentiation degree and lymph node metastasis of ESCC cells to some extent and was involved in the invasion, metastasis, proliferation, and other biological behaviors of ESCC cells, indicating an experimental basis for Annexin-A1 as a molecular marker in the early diagnosis of ESCC and the prediction of cell metastasis, invasion, and differentiation degree. [ABSTRACT FROM AUTHOR]

The present study aimed to establish esophageal squamous carcinoma cell (ESCC) sublines with different invasive and metastatic potentials. Gene microarrays were used for differential gene screening with the establishment of ESCC invasive metastatic gene expression profiles. Some differential gene expressions were validated. Parent line Eca109-T0 was screened in a Transwell chamber to establish Eca109-T4 with high invasion and metastasis. The migrative and proliferative capacities of ESCCs were compared. The Eca109-T0 and Eca109-T4 cell lines were taken as the research objects and were hybridized with gene chips to obtain cell sublines for the screening of differential genes of ESCCs with varying invasive and metastatic potentials. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) clustering analyses were conducted. Some differential genes (HSP90AA1, ANXA1, YWHAB, CXCR7, SDC2, and TNFRSF10D messenger ribonucleic acid) were validated by qualitative real-time polymerase chain reaction and Western blot analysis. As a result, some Eca109-T4 ESCC sublines with high invasive and metastatic potential were screened in a Transwell chamber. The gene chip analysis screened out 326 differential genes, of which 123 were upregulated and 203 were downregulated by Eca109-T4. The GO cluster analysis indicated that the genes were in the cytoplasm, nucleus, and cytosol. The molecular functions of these genes involved the binding of proteins and metal ions and participation in biological processes, including cell signal transduction, transcription, and apoptosis. The KEGG clustering showed that these genes were mainly involved in signaling pathways, such as actin cytoskeleton regulation, the mitogen-activated protein kinase pathway, and the cancer pathway. The validation results were basically consistent with the gene microarray screening results. In Eca109-T4 and CE81T-4, HSP90AA1, YWHAB, and CXCR7 were highly expressed, while the expression of ANXA1 was low. In conclusion esophageal squamous carcinoma cell models with different invasive and metastatic potentials were established. The establishment of differential gene expression profiles for invasion and metastasis together with a bioinformatics analysis provided rich information for studies related to ESCC invasion and metastasis. HSP90a, 14-3-3b, and CXCR7 were highly expressed in ESCCs with high invasion and metastasis, while Annexin A1 was highly expressed in ESCCs with low metastasis. [ABSTRACT FROM AUTHOR]

The article examines the impact of epigallocatechin-3-gallate (EGCG) on proliferation as well as apoptosis of human gastric cancer SGC7901 cells in case of a hypoxic condition. The rise in the concentration of EGCG was found to block proliferation of the cancer cells under a hypoxia condition. Well-grown cells in the logarithmic expansion phase were chosen for the study.

OBJECTIVE: Cullin 4B (CUL4B) is a component of the Cullin 4B-Ring E3 ligase complex (CRL4B) that plays a role in proteolysis and is implicated in tumorigenesis. However, little is known about CUL4B function in human brain tumors, including glioma. MATERIALS AND METHODS: Here, to investigate the involvement of CUL4B in glioma tumorigenesis, endogenous CUL4B expression was depleted in glioblastoma cell lines U87 and U251 by RNA interference (RNAi). RESULTS: Knockdown of CUL4B via shRNAdelivering lentiviruses significantly decreased cell proliferation and colony formation, causing G1 phase cell cycle arrest in both cell lines via down-regulation of cyclin D1 and up-regulation of p16.While increasing the expression of the tumor suppressor PTEN, CUL4B knockdown alleviated in vivo tumorigenesis in glioma xenograft nude mice and impeded cell migration via suppression of MMP-9. CONCLUSIONS: Therefore, knockdown of CUL4B is likely to provide a novel alternative for targeted therapy of glioma deserving further investigation. [ABSTRACT FROM AUTHOR]