Activation and the interaction of proapoptotic genes in modulating sensitivity to anticancer drugs in gastric cancer cells.

1999 ◽  
Author(s):  
R Kim ◽  
Y Ohi ◽  
H Inoue ◽  
T Toge
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Anticancer Drugs ◽  
Gastric Cancer Cells

scholarly journals PTEN/MMAC1 enhances the growth inhibition by anticancer drugs with downregulation of IGF-II expression in gastric cancer cells

2005 ◽  
Vol 37 (5) ◽  
pp. 391-398 ◽  
Author(s):  
Pyoung Han Hwang ◽  
Sun Young Kim ◽  
Jung Chang Lee ◽  
Sun Jun Kim ◽  
Ho Keun Yi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Anticancer Drugs ◽  
Gastric Cancer Cells

scholarly journals The CAGE–MiR-181b-5p–S1PR1 Axis Regulates Anticancer Drug Resistance and Autophagy in Gastric Cancer Cells

2021 ◽  
Vol 9 ◽  
Author(s):  
Minjeong Yeon ◽  
Youngmi Kim ◽  
Deepak Pathak ◽  
Eunju Kwon ◽  
Dong Young Kim ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Anticancer Drugs ◽  
Anticancer Drug ◽  
Autophagic Flux ◽  
Gastric Cancer Cells ◽  
Ags Cells ◽  
Promoter Sequences ◽  
Anticancer Drug Resistance

Cancer-associated gene (CAGE), a cancer/testis antigen, has been known to promote anticancer drug resistance. Since the underlying mechanisms of CAGE-promoted anticancer drug resistance are poorly understood, we established Anticancer drug-resistant gastric cancer cells (AGSR) to better elucidate possible mechanisms. AGSR showed an increased expression level of CAGE and autophagic flux compared with anticancer drug-sensitive parental gastric cancer cells (AGS cells). AGSR cells showed higher invasion potential, growth rate, tumor spheroid formation, and angiogenic potential than AGS cells. CAGE exerted effects on the response to anticancer drugs and autophagic flux. CAGE was shown to bind to Beclin1, a mediator of autophagy. Overexpression of CAGE increased autophagic flux and invasion potential but inhibited the cleavage of PARP in response to anticancer drugs in CAGE CRISPR–Cas9 cell lines. TargetScan analysis was utilized to predict the binding of miR-302b-5p to the promoter sequences of CAGE, and the results show that miR-302b-5p directly regulated CAGE expression as illustrated by luciferase activity. MiR-302b-5p regulated autophagic flux and the response to anticancer drugs. CAGE was shown to bind the promoter sequences of miR-302b-5p. The culture medium of AGSR cells increased CAGE expression and autophagic flux in AGS cells. ImmunoEM showed CAGE was present in the exosomes of AGSR cells; exosomes of AGSR cells and human recombinant CAGE protein increased CAGE expression, autophagic flux, and resistance to anticancer drugs in AGS cells. MicroRNA array revealed miR-181b-5p as a potential negative regulator of CAGE. MiR-181b-5p inhibitor increased the expression of CAGE and autophagic flux in addition to preventing anticancer drugs from cleaving poly(ADP-ribose) polymerase (PARP) in AGS cells. TargetScan analysis predicted sphingosine 1-phosphate receptor 1 (SIPR1) as a potential target for miR-181b-5p. CAGE showed binding to the promoter sequences of S1PR1. The downregulation or inhibition of S1PR1 led to decreased autophagic flux but enhanced the sensitivity to anticancer drugs in AGSR cells. This study presents a novel role of the CAGE–miR-181b-5p–S1PR1 axis in anticancer drug resistance and autophagy.

Regulation of human peptide transporter 1 (PEPT1) in gastric cancer cells by anticancer drugs

2005 ◽  
Vol 230 (1) ◽  
pp. 72-80 ◽  
Author(s):  
Mayumi Inoue ◽  
Tomohiro Terada ◽  
Masahiro Okuda ◽  
Ken-ichi Inui
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Anticancer Drugs ◽  
Peptide Transporter ◽  
Gastric Cancer Cells ◽  
Peptide Transporter 1

Alpha-fetoprotein producing gastric cancer cells lack transcription factor AT-motif binding factor 1 (ATBF1)

2001 ◽  
Vol 120 (5) ◽  
pp. A31-A31
Author(s):  
H KATAOKA ◽  
T JOH ◽  
T OHSHIMA ◽  
Y ITOH ◽  
K SENOO ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Transcription Factor ◽  
Cancer Cells ◽  
Alpha Fetoprotein ◽  
Gastric Cancer Cells ◽  
Binding Factor

Distinct mechanism of helicobacter pylori-mediated NF-κB activation between gastric cancer cells, MKN45 and monocystic cells, THP-1

2001 ◽  
Vol 120 (5) ◽  
pp. A82-A82 ◽  
Author(s):  
S MAEDA ◽  
Y MITSUNO ◽  
Y HIRATA ◽  
M AKANUMA ◽  
H YOSHIDA ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Distinct Mechanism

Hepatocyte Growth Factor Promotes Cell Survival by Phosphorylation of BAD in Gastric Cancer Cells

2008 ◽  
Vol 17 (1) ◽  
pp. 23-32 ◽  
Author(s):  
Kyung Hee Lee ◽  
Eun Young Choi ◽  
Min Kyoung Kim ◽  
Myung Soo Hyun ◽  
Jong Ryul Eun ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Cell Survival ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Hepatocyte Growth
Sign in / Sign up

Export Citation Format

Share Document