As with recent studies of similar arene–Ru complexes, the inhibition of cell growth by metalla-bowls was established against SK-hep-1 (liver cancer), AGS (gastric cancer), and HCT-15 (colorectal cancer) human cancer cell lines.
Gastric cancer (AGS, SNU601, MKN1, and MKN28) and CRC (CoLo320, SW48, HT29, and HCT8) cell lines were treated with 0.2 μM simvastatin alone, or in combination with 0 to 4 Gy of radiation, and subjected to clonogenic survival and proliferation assays in vitro.
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.
To define the inhibitory and pro-apoptotic effects of the two PI3K inhibitors BEZ235 and BKM120 in three human colon cancer (HT-29, HCT-116 and DLD-1) and three gastric cancer (NCI-n87, AGS and MKN-45), cell lines with different PIK3CA gene mutation status were used.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Furthermore, leptin induced GC cell (AGS and MKN-45) migration by upregulating ICAM-1, and knockdown of ICAM-1 by small interference RNA (siRNA) blocked this process.
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.
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.
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.
To investigate the possible mechanisms underlying responses of gastric cancer (GC) cells to AG490, a specific JAK2 inhibitor, human GC cell lines SGC7901 and AGS were used.
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.
Furthermore, AdVTIPE2 treatment obviously suppressed the growth of AGSgastric cancer subcutaneously xenografted tumors implanted in athymic BALB/c nude mice in vivo.