scholarly journals Possible involvement of persistent activity of the mammalian target of rapamycin pathway in the cisplatin resistance of AFP-producing gastric cancer cells

2007 ◽  
Vol 6 (7) ◽  
pp. 1036-1043 ◽  
Author(s):  
Shigeyuki Kamata ◽  
Takashi Kishimoto ◽  
Soichi Kobayashi ◽  
Masaru Miyazaki ◽  
Hiroshi Ishikura
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Mammalian Target Of Rapamycin ◽  
Target Of Rapamycin ◽  
Persistent Activity ◽  
Gastric Cancer Cells

scholarly journals Pharmacologic synergy between dual phosphoinositide-3-kinase and mammalian target of rapamycin inhibition and 5-Fluorouracil inPIK3CAmutant gastric cancer cells

2012 ◽  
Vol 13 (1) ◽  
pp. 34-42 ◽  
Author(s):  
Bhaskar Bhattacharya ◽  
Mohamed Akram ◽  
Indirikumar Balasubramanian ◽  
Kimberley K.Y. Tam ◽  
King X. Koh ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Mammalian Target Of Rapamycin ◽  
Target Of Rapamycin ◽  
Gastric Cancer Cells ◽  
Phosphoinositide 3 Kinase

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.

miR-21 confers cisplatin resistance in gastric cancer cells by regulating PTEN

Toxicology ◽  
2013 ◽  
Vol 306 ◽  
pp. 162-168 ◽  
Author(s):  
Shou-mei Yang ◽  
Cheng Huang ◽  
Xiao-feng Li ◽  
Ming-zhe Yu ◽  
Yong He ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Gastric Cancer Cells

scholarly journals RNF138 confers cisplatin resistance in gastric cancer cells via activating Chk1 signaling pathway

2018 ◽  
Vol 19 (12) ◽  
pp. 1128-1138 ◽  
Author(s):  
Yalan Lu ◽  
Deqiang Han ◽  
Wenjie Liu ◽  
Rong Huang ◽  
Jinhuan Ou ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Cisplatin Resistance ◽  
Gastric Cancer Cells

scholarly journals MiR-99a and MiR-491 Regulate Cisplatin Resistance in Human Gastric Cancer Cells by Targeting CAPNS1

2016 ◽  
Vol 12 (12) ◽  
pp. 1437-1447 ◽  
Author(s):  
Yajie Zhang ◽  
Wenxia Xu ◽  
Pan Ni ◽  
Aiping Li ◽  
Jianwei Zhou ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells

scholarly journals miR-106a confers cisplatin resistance by regulating PTEN/Akt pathway in gastric cancer cells

2013 ◽  
Vol 45 (11) ◽  
pp. 963-972 ◽  
Author(s):  
Y. Fang ◽  
H. Shen ◽  
H. Li ◽  
Y. Cao ◽  
R. Qin ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Akt Pathway ◽  
Gastric Cancer Cells

scholarly journals MCM3AP‑AS1 promotes cisplatin resistance in gastric cancer cells via the miR‑138/FOXC1 axis

2021 ◽  
Vol 21 (3) ◽  
Author(s):  
Han Sun ◽  
Ping Wu ◽  
Bao Zhang ◽  
Xia Wu ◽  
Weixu Chen
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Gastric Cancer Cells

scholarly journals Mitochondrial dysfunction enhances cisplatin resistance in human gastric cancer cells via the ROS-activated GCN2-eIF2α-ATF4-xCT pathway

Oncotarget ◽  
2016 ◽  
Vol 7 (45) ◽  
pp. 74132-74151 ◽  
Author(s):  
Sheng-Fan Wang ◽  
Meng-Shian Chen ◽  
Yueh-Ching Chou ◽  
Yune-Fang Ueng ◽  
Pen-Hui Yin ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Mitochondrial Dysfunction ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells

LncRNA-SNHG7 interferes with miR-34a to de-sensitize gastric cancer cells to cisplatin

2020 ◽  
pp. 1-11
Author(s):  
Li-Juan Pei ◽  
Peng-Jun Sun ◽  
Kui Ma ◽  
Yan-Yan Guo ◽  
Ling-Yan Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Luciferase Assay ◽  
Gastric Cancer Cells ◽  
Non Coding Rna ◽  
Important Regulator ◽  
Cancer Tissues ◽  
Long Non Coding Rna ◽  
Resistant Cells

Gastric cancer (GC) remains poor prognosis and survival issues due to the resistance of chemotherapies, such as cisplatin. The long non-coding RNA small nucleolar RNA host gene 7 (lncRNA-SNHG7) is known as an oncogenic molecule in diverse cancers. Here, we demonstrate that SNHG7 was significantly upregulated in gastric cancer and positively correlated with cisplatin resistance of gastric cancer cells that SNHG7 was significantly upregulated in cisplatin resistant cells. Silencing SNHG7 dramatically sensitized cisplatin resistant cells. In contrast, a negative correlation between lncRNA-SNHG7 and miR-34a was found that miR-34a was downregulated in gastric cancer patient tissues and significantly sensitized cisplatin resistant gastric cancer cells. Intriguingly, bioinformatical analysis indicated miR-34a has putative biding site for SNHG7 and such negative association between SNHG7 and miR-34a was verified in gastric cancer tissues. The cisplatin resistant cells displayed increased glycolysis rate and SNHG7 promoted cellular glycolysis rate of gastric cancer cells. Luciferase assay illustrated LDHA, a glycolysis enzyme, was the direct target of miR-34a. Importantly, inhibiting SNHG7 successfully suppressed LDHA expressions and sensitized cisplatin resistant cells and such inhibitory effects could be recovered by further anti-miR-34a. These findings suggest an important regulator mechanism for the SNHG7-mediated cisplatin resistance via miR-34a/LDHA-glycolysis axis.

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