scholarly journals Exosomal transfer of tumor-associated macrophage-derived miR-21 confers cisplatin resistance in gastric cancer cells

Author(s):  
Peiming Zheng ◽  
Lei Chen ◽  
Xiangliang Yuan ◽  
Qin Luo ◽  
Yi Liu ◽  
...  
Toxicology ◽  
2013 ◽  
Vol 306 ◽  
pp. 162-168 ◽  
Author(s):  
Shou-mei Yang ◽  
Cheng Huang ◽  
Xiao-feng Li ◽  
Ming-zhe Yu ◽  
Yong He ◽  
...  

2018 ◽  
Vol 19 (12) ◽  
pp. 1128-1138 ◽  
Author(s):  
Yalan Lu ◽  
Deqiang Han ◽  
Wenjie Liu ◽  
Rong Huang ◽  
Jinhuan Ou ◽  
...  

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. e13553-e13553
Author(s):  
Takatsugu Ishimoto ◽  
Masayuki Watanabe ◽  
Masaaki Iwatsuki ◽  
Satoshi Ida ◽  
Yohei Nagai ◽  
...  

e13553 Background: CD44 has recently been identified as one of the cell surface markers associated with cancer stem cells (CSCs) in several types of tumor. We have reported the functional role of CD44 variant isoform in the maintenance of low reactive oxygen species (ROS) levels in gastrointestinal cancer cells. Previous studies demonstrated that tumor associated macrophage promotes tumor progression, but the functional role for macrophage in the regulation of CSC marker expression is not known. Methods: We analysed the relationship of CSCs and macrophage infiltration in gastric cancer cell lines and human gastric cancer samples. Results: Here, we showed activated macrophage by LPS and IFNγ produces inflammatory cytokines and chemokines, and these macrophage express CD68 and CD163, which are known as specific markers for pan-macrophage and M2 macrophage. we found that co-culture with activated macrophage triggers the CD44 and Bmi1 expression in gastric cancer cells and promote stem-like property that possess sphere-forming ability. Furthermore, we investigated the relation between CD44 expression and infiltrated macrophage in human gastric cancer. The staining patterns of CD44, Bmi1 and macrophage specific markers (CD68 and CD163) were significantly correlated in tumorous tissues of human gastric adenocarcinoma. Conclusions: These findings establish inflammatory cytokines, which producted from activated macrophage, induce the CD44 and Bmi1 expression in gastric cancer cells. These findings revealed that a role for tumor associated macrophage in the expansion of gastric cancer stem-like cells and subsequent malignant progression.


2016 ◽  
Vol 12 (12) ◽  
pp. 1437-1447 ◽  
Author(s):  
Yajie Zhang ◽  
Wenxia Xu ◽  
Pan Ni ◽  
Aiping Li ◽  
Jianwei Zhou ◽  
...  

2013 ◽  
Vol 45 (11) ◽  
pp. 963-972 ◽  
Author(s):  
Y. Fang ◽  
H. Shen ◽  
H. Li ◽  
Y. Cao ◽  
R. Qin ◽  
...  

2021 ◽  
Vol 21 (3) ◽  
Author(s):  
Han Sun ◽  
Ping Wu ◽  
Bao Zhang ◽  
Xia Wu ◽  
Weixu Chen

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 ◽  
...  

2020 ◽  
pp. 1-11
Author(s):  
Li-Juan Pei ◽  
Peng-Jun Sun ◽  
Kui Ma ◽  
Yan-Yan Guo ◽  
Ling-Yan Wang ◽  
...  

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.


2020 ◽  
Vol Volume 13 ◽  
pp. 10877-10887
Author(s):  
Zhe Song ◽  
Nan Jia ◽  
Wei Li ◽  
Xiao-Yu Zhang

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