scholarly journals A Feedback Loop Regulation Of LINC01433 And YAP Promotes Malignant Behavior In Gastric Cancer Cells

2019 ◽  
Vol Volume 12 ◽  
pp. 7949-7962 ◽  
Author(s):  
Cao Zhang ◽  
Haiquan Qian ◽  
Ke Liu ◽  
Wei Zhao ◽  
Lei Wang
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Feedback Loop ◽  
Gastric Cancer Cells ◽  
Malignant Behavior

LncRNA LINC00470 promotes the degradation of PTEN mRNA to facilitate malignant behavior in gastric cancer cells

2020 ◽  
Vol 521 (4) ◽  
pp. 887-893 ◽  
Author(s):  
Jijun Yan ◽  
Xiufang Huang ◽  
Xiongjie Zhang ◽  
Zhijie Chen ◽  
Chao Ye ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Pten Mrna ◽  
Malignant Behavior

scholarly journals A self-enforcing HOXA11/Stat3 feedback loop promotes stemness properties and peritoneal metastasis in gastric cancer cells

Theranostics ◽  
2019 ◽  
Vol 9 (25) ◽  
pp. 7628-7647 ◽  
Author(s):  
Chao Wang ◽  
Min Shi ◽  
Jun Ji ◽  
Qu Cai ◽  
Jinling Jiang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Peritoneal Metastasis ◽  
Feedback Loop ◽  
Gastric Cancer Cells

scholarly journals Epigenetically deregulated miR-200c is involved in a negative feedback loop with DNMT3a in gastric cancer cells

2016 ◽  
Vol 36 (4) ◽  
pp. 2108-2116 ◽  
Author(s):  
Yingfei Li ◽  
Yuqiang Nie ◽  
Sanfang Tu ◽  
Hong Wang ◽  
Yongjian Zhou ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Negative Feedback Loop ◽  
Gastric Cancer Cells

scholarly journals Effects and Mechanism of Dihydroartemisinin on Malignant Behavior of Cisplatin-Resistant Gastric Cancer Cells

2018 ◽  
Vol 4 (Supplement 2) ◽  
pp. 215s-215s
Author(s):  
S. Zhang ◽  
R. Feng ◽  
F. Yuan ◽  
X. Chen ◽  
N. Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Expression Level ◽  
Dependent Manner ◽  
Cancer Resistance ◽  
Gastric Cancer Cells ◽  
Concentration Dependent Manner ◽  
Expression Levels ◽  
Malignant Behavior

Background: Studies showed that dihydroartemisinin (DHA) has significant antitumor effects. However, there have been no relevant reports on gastric cancer resistance to DHA. Aim: To investigate the influence of DHA on the malignant behavior of cisplatin (DDP)-resistant gastric cancer cells SGC7901/DDP and the possible molecular mechanism. Methods: The IC50 of DHA against SGC7901/DDP cells at 48 h was obtained with CCK-8. DHA was used against SGC7901/DDP, with IC50 concentration at 0 µmol/L, 0.5-fold, onefold, and twofold respectively. Then the proliferation activity of SGC7901/DDP from day 1 to day 5 was detected by CCK-8. At 48 h after DHA treatment, we observed apoptosis, invasion, and migration, evaluated autophagy, and detected the expression level of protein related to the regulation of autophagy, apoptosis, angiogenesis and lymphangiogenesis with Western blot. The influence of DHA on cisplatin resistance of SGC7901/DDP was detected through sensitization test and the evaluation of p-gp expression level. Results: The IC50 concentration of DHA against SGC7901/DDP cells at 48 h is 70 µmol/L. DHA significantly inhibited the proliferation of SGC7901/DDP, which was time- and concentration-dependent (all P < 0.05). After having been treated for 48 h by increasing concentrations of DHA (0, 35, 70 and 140 µmol/L), the apoptosis rate increased and the penetrating cell number and scratch healing rate significantly decreased (all P < 0.05). The expression levels of Beclin1 and LC3-II/LC3-I which were corrected with autophagy, and the formation of autophagosomes and autophagous vacuoles increased in a concentration-dependent manner (all P < 0.05). The total PI3K, Akt, and mTOR expression levels did not significantly change, but their phosphorylated products (PI3P, p-Akt [Ser473], and p-mTOR) showed concentration-dependent decreases (all P < 0.05). The expression of caspases-8/9/3 protein significantly increased while the expression of VEGF-A、VEGF-C protein decreased (all P < 0.05). DHA could reverse the resistance of SGC7901/DDP cells to cisplatin after DHA treatment at a nontoxic dose (15.23 µg/mL) with a reversal rate of 2.95. After DHA treatment at different concentrations for 48 h, the expression of p-gp was significantly reduced in a concentration-dependent manner ( P < 0.05). Conclusion: DHA significantly inhibited proliferation, promoted programmed death, and had anti-invasion and antimetastatic effects on SGC7901/DDP cells, probably by upregulating autophagy-related Beclin1 and LC3-II expression and by inhibiting the antiautophagy signaling pathway PI3K/AKT/mTOR, thus promoting autophagic death. In addition, DHA induced caspase-dependent and mitochondrial pathway apoptosis in SGC7901/DDP cells, and reduced VEGF-A and VEGF-C activity to promote antiangiogenesis and antilymphangiogenesis. Furthermore, DHA effectively reversed the cisplatin resistance of gastric cancer cell by inhibiting p-gp expression.

scholarly journals CXCR1 promotes malignant behavior of gastric cancer cells in vitro and in vivo in AKT and EKR1/2 phosphorylation

2016 ◽  
Vol 48 (5) ◽  
pp. 2184-2196 ◽  
Author(s):  
JUNPU WANG ◽  
WANMING HU ◽  
XIAOYING WU ◽  
KUANSONG WANG ◽  
JUN YU ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Malignant Behavior

scholarly journals Exosomal miR-27a Derived from Gastric Cancer Cells Regulates the Transformation of Fibroblasts into Cancer-Associated Fibroblasts

2018 ◽  
Vol 49 (3) ◽  
pp. 869-883 ◽  
Author(s):  
Jingya Wang ◽  
Xuwen Guan ◽  
Yue Zhang ◽  
Shaohua Ge ◽  
Le Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Biological Behavior ◽  
Transport Systems ◽  
Cancer Associated Fibroblasts ◽  
Gastric Cancer Cells ◽  
Downstream Target ◽  
Malignant Behavior

Background/Aims: The malignant biological behavior of gastric cancer(GC) is not only determined by cancer cells alone, but also closely regulated by the microenvironment. Fibroblasts represent a large proportion of the components in the tumor microenvironment, and they promote the development of disease. Currently, accumulating evidence suggests that exosomes can function as intercellular transport systems to relay their contents, especially microRNAs(miRNAs). Methods: First, we detected the highly-expressed level of miR-27a in exosomes isolated from gastric cancer cells by qRT-PCR. MiR-27a –over-expressed models in vitro and in vivo were established to investigate the transformation of cancer-associated fibroblasts observed by Western blotting, and the malignant behavior of gastric cancer cells using the methods CCK8 and Transwell. Moreover, the downregulation of CSRP2 in fibroblasts was used to evaluate the promotion of malignancy of gastric cancer using the methods CCK8 and Transwell. Results: In this study, we found a marked high level of miR-27a in exosomes derived from GC cells. miR-27a was found to function an oncogene that not only induced the reprogramming of fibroblasts into cancer-associated fibroblasts(CAFs), but also promoted the proliferation, motility and metastasis of cancer cells in vitro and in vivo. Conversely, CAFs with over-expression of miR-27a could pleiotropically increase the malignant behavior of the GC cells. For the first time, we revealed that CSRP2 is a downstream target of miR-27a. CSRP2 downregulation could increase the proliferation and motility of GC cells. Conclusion: Thus, this report indicates that miR-27a in exosomes derived from GC cells has a crucial impact on the microenvironment and may be used as a potential therapeutic target in the treatment of GC

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