The particles were more toxic to cancer cells than normal cells; the dose of the NPs (4-5 μg ml<sup>-1</sup>), that killed about 75% of the different human cancer cell lines viz, HepG2 (liver cancer), A549 (lung cancer) and AGS (stomach cancer), killed only about 22.5% of the normal cell lines viz, WRL68 (liver) and WI38 (lung).
The present study aimed to detect novel tumor‑associated antigens from the AGSGC cell line, and to identify their associated autoantibodies in sera from patients with GC by proteomics‑based approaches.
FKB is potently cytotoxic to human gastric cancer cells (AGS/NCI-N87/KATO-III/TSGH9201) and mildly toxic towards normal (Hs738) cells and primary mouse hepatocytes.
Carcinomatous and adjacent tissues of 43 GC patients, normal gastric mucosa cell line GES-1 and GC cell lines including AGS, HGC-27, KATO III, NCI-N87, SGC-7901, MKN-45 and MGC-803 were collected.
In this study, we identified that the carcinogenic bacterium H. pylori increased ETS2 transcription factor-mediated Siah1 protein expression in gastric cancer cells (GCCs) MKN45, AGS and Kato III.
<i>In vitro</i> and <i>in vivo</i> experiments demonstrated that silencing <i>MAEL</i> expression in the GC cell lines HGC-27 and AGS inhibits proliferation, colony formation, migration, invasion and growth of xenograft tumors, whereas <i>MAEL</i> overexpression exerts the opposite effects in the normal gastric cell line GES-1.
These findings demonstrate that Tan-IIA inhibits the migration ability of AGS human gastric cancer cells and that decreasing the protein expression of NF-κB-p65, COX-2, and MMP-2, -7 and -9 may be an underlying molecular mechanism.
Whole-genome sequencing was conducted on two gastric cancer (GC) cells, BGC823 and AGS, which do and do not form tumors in nude mice, to identify their genomic differences relevant to natural killer (NK) cells.
Forced expression of miR-124 inhibited GC cell growth, migration and invasion, and induced cell cycle arrest. miR-124 negatively regulated Notch1 signalling by targeting JAG1. miR-124 levels were also shown to be inversely correlated with JAG1 expression in GC.
Furthermore, AdVTIPE2 treatment obviously suppressed the growth of AGSgastric cancer subcutaneously xenografted tumors implanted in athymic BALB/c nude mice in vivo.
Transfection of AGS and MKN7 gastric cancer cells with PGT-specific siRNA led to increased VEGF mRNA and protein expression accompanied by increased PGE2 in the culture media.
Cultured gastric cancer cells (GCCs) MKN45, AGS and Kato III showed significantly induced expression of Siah2, increased invasiveness and migration after being challenged with the pathogen.
Re-expression of RASSF10 in GC cell lines (AGS and MKN45) significantly suppressed cell viability, colony formation, migration and invasion, reduced cells in S phase, accumulated cells in G2 phase and induced cell apoptosis in vitro, and inhibited tumorigenicity in nude mice.
Enhanced gene expression was detected when the HGC27, AGS and BGC823 GC cell lines were treated with the DNA-demethylating agent 5-aza-2'-deoxycytidine.
A co-culture system of OPN+-AGS and U937 cells was designed to study the effect of OPN on the skewing of macrophages toward M2-TAMs for gastric cancer progression in vitro and in vivo.
We characterized the functions of FPRs in GC epithelial cells (MKN28, AGS and MKN45) cultured in vitro by assessing migration, proliferation, resistance to apoptosis and activation of the epithelial-to-mesenchymal transition.
Real-time quantitative reverse transcriptase polymerase chain (qRT-PCR) was used to examine the expression levels of miR-133a in human GC and adjacent non-tumor tissues, as well as in GC cell lines (SGC-7901, BGC-823, MGC-803, and AGS) and a human gastric mucosal epithelial cell line (GES-1).