CPEB1 enhances erastin‐induced ferroptosis in gastric cancer cells by suppressing twist1 expression

IUBMB Life ◽  
2021 ◽  
Author(s):  
Jing Wang ◽  
Tao Wang ◽  
Yang Zhang ◽  
Jiaqi Liu ◽  
Jie Song ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Twist1 Expression

scholarly journals DNA Methylation in the Exon 1 Region and Complex Regulation of Twist1 Expression in Gastric Cancer Cells

PLoS ONE ◽  
2015 ◽  
Vol 10 (12) ◽  
pp. e0145630 ◽  
Author(s):  
Ayuna Sakamoto ◽  
Yoshimitsu Akiyama ◽  
Shu Shimada ◽  
Wei-Guo Zhu ◽  
Yasuhito Yuasa ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Dna Methylation ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Twist1 Expression ◽  
Exon 1 ◽  
Complex Regulation

scholarly journals ETS2 and Twist1 promote invasiveness of Helicobacter pylori-infected gastric cancer cells by inducing Siah2

2016 ◽  
Vol 473 (11) ◽  
pp. 1629-1640 ◽  
Author(s):  
Lopamudra Das ◽  
Shrikant Babanrao Kokate ◽  
Suvasmita Rath ◽  
Niranjan Rout ◽  
Shivaram Prasad Singh ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Twist1 Expression ◽  
H Pylori

H. pylori induce ETS2 and Twist1 expression in the infected GCC. ETS2 and Twist1 transcriptionally activate siah2 in the H. pylori-infected GCCs. H. pylori-mediated Siah2 induction enhances motility and invasiveness of the infected GCCs.

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

Silencing of circRACGAP1 Sensitizes Gastric Cancer Cells to Apatinib via Modulating Autophagy by Targeting miR-3657 and ATG7

2019 ◽  
Author(s):  
Ling Ma ◽  
Zhangding Wang ◽  
Mengyan Xie ◽  
Weiyou Zhu ◽  
Fengming Yang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Gastric Cancer Cells

Effects and Mechanisms of Anlotinib and Dihydroartemisinin Combination Therapy in Ameliorating Malignant Biological Behavior of Gastric Cancer Cells

2020 ◽  
Vol 21 ◽  
Author(s):  
Qiong Luo ◽  
Suyun Zhang ◽  
Donghuan Zhang ◽  
Rui Feng ◽  
Nan Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Chorioallantoic Membrane ◽  
Cell Counting ◽  
Biological Behavior ◽  
Gastric Cancer Cells ◽  
Invasion And Migration ◽  
Apoptosis Related Protein ◽  
And Migration

Background: Gastric cancer(GC) is currently one of the major malignancies that threatens human lives and health. Anlotinib is a novel small-molecule that inhibits angiogenesis to exert anti-tumor effects. However, the function in gastric cancer is incompletely understood. Objective: The aim of the present study was to investigate the anti-tumor effects and molecular mechanisms of anlotinib combined with dihydroartemisinin (DHA) in SGC7901 gastric cancer cells. Method: Different concentrations of anlotinib and DHA were used to treat SGC7901 gastric cancer cells, after which cell proliferation was measured. Drug interactions of anlotinib and DHA were analyzed by the Chou-Talalay method with CompuSyn software. proliferation, apoptosis, invasion, migration, and angiogenesis were measured using the cell counting kit-8 (CCK8) assay, flow cytometry, Transwell invasion assays, scratch assays, and chicken chorioallantoic membrane (CAM) assays. proliferation-associated protein (Ki67), apoptosis-related protein (Bcl-2), and vascular endothelial growth factor A (VEGF-A) were quantified by Western bloting. Results: The combination of 2.5 μmol/L of anlotinib and 5 of μmol/L DHA was highly synergistic in inhibiting cell growth, significantly increased the apoptosis rate and suppressed obviously the invasion and migration capability and angiogenesis of gastric cancer cells. In addition, the expression levels of Ki67, Bcl-2, and VEGF-A, as well as angiogenesis, were significantly decreased in the Combination of drugs compared with in control and either drug alone. Conclusion: The combination of anlotinib and DHA showed synergistic antitumor activity, suggesting their potential in treating patients with gastric cancer.

OSI-027 alleviates oxaliplatin chemoresistance in gastric cancer cells by suppressing P-gp induction

2020 ◽  
Vol 20 ◽  
Author(s):  
En Xu ◽  
Hao Zhu ◽  
Feng Wang ◽  
Ji Miao ◽  
Shangce Du ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Mammalian Target Of Rapamycin ◽  
Cell Counting ◽  
Gastric Cancer Cells ◽  
Ags Cells ◽  
Dual Inhibitor ◽  
Induced Apoptosis

: Gastric cancer is one of the most common malignancies worldwide and the third leading cause of cancer-related death. In the present study, we investigated the potential activity of OSI-027, a potent and selective mammalian target of rapamycin complex 1/2 (mTOR1/2) dual inhibitor, alone or in combination with oxaliplatin against gastric cancer cells in vitro. Cell counting kit-8 assays and EdU staining were performed to examine the proliferation of cancer cells. Cell cycle and apoptosis were detected by flow cytometry. Western blot was used to detect the elements of the mTOR pathway and Pgp in gastric cancer cell lines. OSI-027 inhibited the proliferation of MKN-45 and AGS cells by arresting the cell cycle in the G0/G1 phase. At the molecular level, OSI-027 simultaneously blocked mTORC1 and mTORC2 activation, and resulted in the downregulation of phosphor-Akt, phpspho-p70S6k, phosphor-4EBP1, cyclin D1, and cyclin-dependent kinase4 (CDK4). Additionally, OSI-027 also downregulated P-gp, which enhanced oxaliplatin-induced apoptosis and suppressed multidrug resistance. Moreover, OSI-027 exhibited synergistic cytotoxic effects with oxaliplatin in vitro, while a P-gp siRNA knockdown significantly inhibited the synergistic effect. In summary, our results suggest that dual mTORC1/mTORC2 inhibitors (e.g., OSI-027) should be further investigated as a potential valuable treatment for gastric cancer.

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