We report that Wg treatment inhibited cell viability and induced apoptosis in human GC cell lines AGS and SGC-7901, and also retarded GC tumor growth in xenograft mice in vivo.
We knocked down H19 in AGS and SGC7901 cell lines and found that knocked-down H19 could decrease gastric cancer cell invasion and that metformin could not further decrease invasion after the knock down.
AGS and SGC-7901 cells were treated with β-cryptoxanthin (0-40 μM) and AGS cells were injected in BALB/c (nu/nu) mice to analyze the effect of β-cryptoxanthin on GC.
In vitro assays of the GC cell lines AGS and BGC-823 demonstrated that knockdown of circ-EIF4G3 inhibited cell proliferation, invasion and migration significantly.
Therefore, MALAT1 potentiated autophagy‑related CDDP resistance through suppressing the miR‑30b/ATG5 axis in AGS/CDDP and HGC‑27/CDDP cells, indicating that it may represent a promising target for the reversal of chemoresistance in GC.
The results clearly prove that CH-AuNP increases ROS and induces apoptosis in AGS, suggesting that CH-AuNP may be an effective anticancer drug with no side effects to treat gastric cancer.
Bioinformatics and dual luciferase reporter gene assays were used to analyze the relationship between miR-107 and FAT4. miR-NC, miR-107 inhibitor, pcDNA3.1-FAT4 and siRNA-FAT4 were transfected into AGS and MKN-45 GC cell lines, respectively.
First, short hairpin RNA (shRNA) against BMX-ARHGAP or BMX-ARHGAP were introduced to treat SGC-7901 cells with the highest BMX-ARHGAP among the five GC cell lines (SGC-7901, MKN-45, NCI-N87, SNU-5, and AGS).
The levels of miR-17 and DEDD in GC tissues from patients diagnosed with GC and in five GC cell lines (SGC-7901, MKN-45, HGC-27, BGC823, and AGS) were detected.
In this manuscript we aim to find the molecular processes involved in cisplatin-induced apoptosis in two gastric cancer cell lines with different sensitivity to the treatment: AGS and MKN45.
In this study, we aimed to analyze the effects of mtDNA content on cell surface positivity for anti-CD24 and anti-CD44 antibodies and chemoresistance level in AGS, HGC-27 and MKN-45 gastric cancer (GC) cell lines and to determine a setpoint for mtDNA copy for each cell line.
Furthermore, in vitro assays of the GC cell lines BGC-823 and AGS demonstrated that knockdown of circ_0066444 reduced cell proliferation, invasion, and migration significantly.
Our conceptualization agrees well with our empirical analysis of two modern day NGS (Next-generation sequencing) datasets: an in-house generated dilution miRNA study of two gastric cancer cell lines (NUGC3 and AGS) and a publicly available spike-in miRNA data; Firstly, the finite-size effects causes the deviations of sequencing count data from Zipf's law and issues of reproducibility in sequencing experiments.
The effects on cell viability, cytotoxicity and apoptosis were investigated in breast cancer (MCF-7 and SK-BR3) and gastric cancer (AGS and NCI-N87) cell lines using the ApoTox-Glo and Caspase-Glo assays and qPCR.
The gastric cancer cell lines MGC‑803 and AGS were transfected with GHET1‑directed small interfering RNA (siRNA) and the changes in phenotype and cell‑cycle‑related molecules were assessed.
In this effort, we provided comparative study on optimization of transfection conditions for AGS human gastric cancer cell line using two commercial non-liposomal cationic lipids.
To identify new treatment strategies for gastric cancer and to elucidate the mechanism underlying its pathophysiology, we transfected sh-MARCH8 into the human gastric cancer cell lines MKN-45 and AGS to investigate the roles of MARCH8 in gastric cancer.