Knockdown of ZFX inhibits gastric cancer cell growth in vitro and in vivo via downregulating the ERK-MAPK pathway

2013 ◽  
Vol 337 (2) ◽  
pp. 293-300 ◽  
Author(s):  
Shuai Wu ◽  
Xin-Yuan Lao ◽  
Tian-Tian Sun ◽  
Lin-Lin Ren ◽  
Xuan Kong ◽  
...  
2011 ◽  
Vol 294 (5) ◽  
pp. 781-788 ◽  
Author(s):  
Hui Liu ◽  
Li Xu ◽  
Jian-En Wei ◽  
Mei-Rong Xie ◽  
Shi-E Wang ◽  
...  

Nutrition ◽  
2021 ◽  
pp. 111413
Author(s):  
Qianxiu Li ◽  
Yifan Li ◽  
Houxiang Jiang ◽  
Zhangang Xiao ◽  
Xu Wu ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Shun-Hong Mao ◽  
Chun-Hua Zhu ◽  
Yu Nie ◽  
Jian Yu ◽  
Lei Wang

Gastric cancer is one of the most the prevalent malignancies and the therapeutic strategies for patients with gastric cancer remains limited. Local anesthetic levobupivacaine has demonstrated potential anti-cancer property, but its correlation with gastric cancer and ferroptosis is poor understood. Here, we identified the novel function of levobupivacaine in regulating ferroptosis of gastric cancer cells. The treatment of levobupivacaine suppressed gastric cancer cell viabilities and Edu-positive cell proportions. The gastric cancer cell growth was reduced by levobupivacaine in vivo. Moreover, the treatment of levobupivacaine enhanced erastin-induced inhibitory impact on gastric cancer cell viabilities. The levels of Fe2+/iron and lipid ROS were induced by levobupivacaine in erastin and RSL3-stimulated gastric cancer cells. levobupivacaine-upregulated miR-489-3p enhanced ferroptosis of gastric cancer cells by targeting SLC7A11. MiR-489-3p was involved in levobupivacaine-induced ferroptosis of gastric cancer cells. Levobupivacaine/miR-489-3p/SLC7A11 axis attenuates gastric cancer cell proliferation in vitro. Therefore, we concluded that the local anesthetic levobupivacaine induced ferroptosis of gastric cancer cells to repress gastric cancer cell growth by miR-489-3p/SLC7A11 axis.


2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Liang Sun ◽  
Yizhou Yao ◽  
Ting Lu ◽  
Zengfu Shang ◽  
Shenghua Zhan ◽  
...  

DAB2IP (DOC2/DAB2 interactive protein) is downregulated in several cancer types, and its downregulation is involved in tumor cell proliferation, apoptosis, metastasis, and epithelial-mesenchymal transition (EMT). We aimed to investigate the potential role of DAB2IP in the development and progression of gastric cancer. DAB2IP levels were analyzed in human gastric cancer and adjacent normal tissues by Western blots and immunohistochemistry. Potential roles of DAB2IP in regulating gastric cancer cell growth and metastasis were examined by genetic manipulation in vitro. The molecular signaling was determined to understand the mechanisms of observed DAB2IP effects. DAB2IP level is lower in gastric cancer tissues as compared to paired normal tissues. Knockdown of DAB2IP enhanced gastric cancer cell growth and metastasis in vitro and promoted EMT progress at both protein and mRNA levels. Silencing DAB2IP activated extracellular signal-regulated kinase 1/2 (ERK1/2) pathway, and the enhanced proliferation and migration ability induced by DAB2IP knockdown were reduced after incubation with U0126 in SGC7901 gastric cancer cells. Inhibition of DAB2IP enhances gastric cancer cell growth and metastasis through targeting the ERK1/2 signaling, indicating that it may serve as a potential target for treatment of gastric cancer.


2010 ◽  
Vol 38 (2) ◽  
pp. 949-955 ◽  
Author(s):  
Chun-xiao Xu ◽  
Yun-fei Yan ◽  
Ya-pei Yang ◽  
Bin Liu ◽  
Jia-xuan Xin ◽  
...  

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