A novel protein from Eupolyphaga sinensis inhibits adhesion, migration, and invasion of human lung cancer A549 cells

2013 ◽  
Vol 91 (4) ◽  
pp. 244-251 ◽  
Author(s):  
Feng-xia Wang ◽  
Ning Wu ◽  
Jian-teng Wei ◽  
Jia Liu ◽  
Jin Zhao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
A549 Cell ◽  
High Performance ◽  
Human Lung ◽  
Gel Filtration ◽  
A549 Cells ◽  
Human Lung Cancer ◽  
Migration And Invasion ◽  
Fast Flow ◽  
Novel Protein

Eupolyphaga sinensis Walker is an important insect used in Chinese traditional medicine. In this study, we purified a 72-kDa anticancer protein, designated as EPS72, from this species using ammonium sulfate precipitation, ultrafiltration, CM Sepharose Fast Flow cation exchange, Q Sepharose High Performance (HP) anion exchange, Butyl Sepharose HP hydrophobic chromatography, and Superdex 75 gel filtration chromatographic techniques. EPS72 exhibited a potent anticancer activity against the human lung cancer A549 cell line (IC50, 18.76 μg/mL). Further study showed that EPS72 could induce A549 cell detachment and apoptosis, inhibit cell adhesion to fibronectin and collagen IV, and restrain cell migration and invasion. Moreover, EPS72 significantly decreased the expression of β1-integrin. This study suggests that EPS72 could potentially be developed as a novel anticancer therapeutic agent due to its possible antimetastatic activity.

Astragaloside IV inhibits migration and invasion in human lung cancer A549 cells via regulating PKC-α-ERK1/2-NF-κB pathway

2014 ◽  
Vol 23 (1) ◽  
pp. 304-313 ◽  
Author(s):  
Xudong Cheng ◽  
Junfei Gu ◽  
Minghua Zhang ◽  
Jiarui Yuan ◽  
Bingjie Zhao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Human Lung ◽  
A549 Cells ◽  
Human Lung Cancer ◽  
Migration And Invasion ◽  
Astragaloside Iv

RNA interference-mediated knockdown of RhoGDI2 induces the migration and invasion of human lung cancer A549 cells via activating the PI3K/Akt pathway

Tumor Biology ◽  
2014 ◽  
Vol 36 (1) ◽  
pp. 409-419 ◽  
Author(s):  
Huiyan Niu ◽  
Baogang Wu ◽  
Yang Peng ◽  
Hongfang Jiang ◽  
Yi Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Rna Interference ◽  
Human Lung ◽  
A549 Cells ◽  
Human Lung Cancer ◽  
Akt Pathway ◽  
Migration And Invasion

Cochinchina MomordicaSeed Suppresses Proliferation and Metastasis in Human Lung Cancer Cells by Regulating Multiple Molecular Targets

2015 ◽  
Vol 43 (01) ◽  
pp. 149-166 ◽  
Author(s):  
Yang Shen ◽  
Linyi Meng ◽  
Huajun Sun ◽  
Yizhun Zhu ◽  
Hongrui Liu
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Human Lung ◽  
A549 Cells ◽  
Molecular Targets ◽  
Human Lung Cancer ◽  
Migration And Invasion ◽  
Human Lung Cancer Cells ◽  
Proliferation And Metastasis ◽  
Specific Inhibitors

Cochinchina Momordica Seed, which is the dried ripe seed of Momordica cochinchinensis (Lour.) Spreng, has been used as a mainly anticancer ingredient for many years in China. This study aims at investigating the roles of an ethanol-soluble extract of Cochinchina Momordica Seed (ECMS) in suppressing the proliferation and metastasis of human lung cancer cells, and further elucidating underlying molecular mechanisms. Our researches suggest that ECMS dose-dependently decreased the survival rates of A549 and H1299 cells, and inhibited the migration and invasion in A549 cells. ECMS-induced apoptosis was accompanied by up-regulation of p53, Bax and the down-regulation of Bcl-2, PI-3K/Akt signal pathway, and resulted in the dissipation of mitochondrial membrane potential (ΔΨm) and sequentially activated caspase-3 cascade. Pre-treated with specific inhibitors, LY294002 (PI-3K inhibitor) and BAY11-7082 (NF-κB inhibitor) could enhance the anti-proliferation effects of ECMS on A549 cells. Furthermore, ECMS could increase the level of E-cadherin and decrease of the level of STAT-3 and MMP-2, and scarcely affected the expression of VEGF, and resulted in the inhibition of migration and invasion. Pre-treated with specific inhibitors, WP1066 (STAT-3 inhibitor) and TIMP-2 (MMP-2 inhibitor) could enhance the inhibitory effects of ECMS on migration. In conclusion, the current data demonstrated ECMS inhibited the proliferation of A549 cells by inducing apoptosis, at least partly through the activation of p53 and inactivation of PI-3K/Akt signaling. STAT-3 and MMP-2 pathways may be partly involved in anti-metastasis activities of ECMS. Hence, ECMS might be a promising candidate for the therapy of the non-small cell lung cancer by regulating multiple molecular targets.

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