Inhibition of fatty acid synthase suppresses U-2 OS cell invasion and migration via downregulating the activity of HER2/PI3K/AKT signaling pathway in vitro

2013 ◽  
Vol 440 (2) ◽  
pp. 229-234 ◽  
Author(s):  
Tao Fang Wang ◽  
Heng Wang ◽  
Ai Fen Peng ◽  
Qing Feng Luo ◽  
Zhi Li Liu ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Signaling Pathway ◽  
Cell Invasion ◽  
Fatty Acid Synthase ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Invasion And Migration ◽  
And Migration

miR-340 Inhibits the Development of Hepatocellular Carcinoma by Down-Regulating Akt Signaling Pathway

2021 ◽  
Vol 11 (9) ◽  
pp. 1785-1791
Author(s):  
Tangpeng Xu ◽  
Changli Ruan ◽  
Xu Bin ◽  
Mengxue Hu
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Pathological Grade ◽  
Akt Signaling Pathway ◽  
Invasion And Migration ◽  
Proliferation Ability ◽  
And Migration ◽  
Cancer Tissues

Hepatocellular carcinoma (HCC) is a serious threat to human health. miR-340 participates in HCC pathogenesis, but its specific mechanism is not completely clear. Therefore, our study assessed the mechanism by how miR-340 involves in HCC. The cancer tissues and paracancerous tissues of HCC patients were collected. miR-340 mimics/NC and Akt siRNA were transfected into HepG2 cells followed by analysis of miR-304 and EMT-related molecules expression by Real-time PCR, cell invasion and migration by Transwell assay, cell proliferation ability by CCK8 assay as well as p-Akt and p-mTOR level by Western blot. miR-340 in HCC tissues was significantly downregulated compared to adjacent tissues (P <0.001). With increased pathological grade, miR-340 expression was decreased gradually. p-Akt and p-mTOR in HCC tissues was significantly upregulated and elevated gradually with increased pathological grade. p-Akt and p-mTOR was negatively associated with miR-340 (P <0.001). After overexpression of miR-340, HepG2 cell proliferation, invasion, migration and epithelialization were significantly inhibited, and p-Akt and p-mTOR was reduced. When Akt expression was interfered with siRNA, cell proliferation and epithelialization was further inhibited. miR-340 inhibits the development of hepatocellular carcinoma through Akt signaling pathway.

PdpaMn inhibits fatty acid synthase-mediated glycolysis by down-regulating PI3K/Akt signaling pathway in breast cancer

2020 ◽  
Vol 31 (10) ◽  
pp. 1046-1056 ◽  
Author(s):  
Eric Achiborebador Okrah ◽  
Qiang Wang ◽  
Hexiu Fu ◽  
Qiuyun Chen ◽  
Jing Gao
Keyword(s):  
Breast Cancer ◽  
Fatty Acid ◽  
Signaling Pathway ◽  
Fatty Acid Synthase ◽  
Akt Signaling ◽  
Akt Signaling Pathway

scholarly journals TRIM31 promotes proliferation, invasion and migration of glioma cells through Akt signaling pathway

Neoplasma ◽  
2019 ◽  
Vol 66 (05) ◽  
pp. 727-735
Author(s):  
G. Shi ◽  
C. Lv ◽  
Z. Yang ◽  
T. Qin ◽  
L. Sun ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Glioma Cells ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Invasion And Migration ◽  
And Migration

scholarly journals IGF2BP2 Promotes the Proliferation, Invasion and Migration of Esophageal Carcinoma Cells via Activation of the PI3K/AKT/EMT Signaling Pathway

2021 ◽  
Author(s):  
Wenbin Shu ◽  
YuJing Lin ◽  
Yan Yan ◽  
YaoHui Sun ◽  
XiangWen Wu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration ◽  
Mrna Binding

Abstract BackgroundInsulin-like growth factor 2 (IGF2) mRNA-binding protein 2 (IGF2BP2), as a m6A “reader”, is known to be an oncogene, and its expression is elevated in multiple tumors. However, the role of IGF2PB2 in esophageal squamous cell carcinoma (ESCC) is still unclear. MethodsThis study aims to investigate the role of IGF2PB2 expression in ESCC proliferation, invasion and migration as well as the possible mechanism. IGF2BP2 expression was found to be elevated in ESCC tissues by qRT-PCR, western blotting, and immunohistochemical (IHC) staining. ResultsKnocking down IGF2BP2 expression prevented the proliferation, invasion, migration and epithelial-mesenchymal transition (EMT) of KYSE450 and TE1 cells. Knocking out IGF2BP2 reduced tumorigenesis in vivo. Overexpression of IGF2BP2 was performed, and it was proven that IGF2BP2 had an oncogenic effect in KYSE450 and TE1 cells. Moreover, LY294002, a highly selective inhibitor of PI3K, reversed the effect of IGF2BP2 overexpression on EMT processes. All these results show that the effects of IGF2BP2 on oncogenesis and EMT were clearly exerted via the PI3K/AKT signaling pathway. ConclusionsIn conclusion, this study demonstrates that the oncogenic function of IGF2BP2 is mediated by the PI3K/AKT signaling pathway and is related to EMT in ESCC. In addition, IGF2BP2 can serve as a diagnostic and oncotherapeutic marker in further studies.

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