Abstract 1050: Alvespimycin (17-DMAG) blocks TGFβ-induced EMT and migration in A549 lung cancer cells

2014 ◽  
Author(s):  
Edna Gordian ◽  
Eric Welsh ◽  
Teresita Muñoz-Antonia
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
And Migration ◽  
A549 Lung

Effects of Intermittent Cisplatin Intervention on 6PGD Levels and Tumor Growth and Migration in A549 Lung Cancer Cells

2021 ◽  
Vol 8 ◽  
Author(s):  
WU Qiang ◽  
TANG Lin-dong ◽  
WU Yan-hui ◽  
LI Qiang ◽  
YU Li
Keyword(s):  
Lung Cancer ◽  
Tumor Growth ◽  
Western Blot ◽  
Cancer Cells ◽  
A549 Cells ◽  
Lung Cancer Cells ◽  
Migration Ability ◽  
Western Blot Method ◽  
And Migration ◽  
A549 Lung

Aim: To investigate the changes of A549 protein 6PGD expression, tumor growth and migration, NADPH and ROS levels in lung cancer cells after intermittent intervention with DDP. Methods: The sensitivity of A549 cells to DDP was detected by cck-8 method, A549 cells were treated by DDP intermitten, 6PGD protein expression was detected by Western blot method, and the ROS level of A549 cells was determined by ROS kit. NADPH levels of A549 cells were determined by NADPH kit. Result: After DDP intermittent intervention, the expression of 6PGD protein in lung cancer cells A549 was increased, the growth and migration of A549 cells were significantly inhibited, and ROS and NADPH levels were significantly increased. Conclusion: 6PGD were upregulated in after DDP intermittent intervention and affected the migration ability in lung cancer cells.

scholarly journals Activation of NLRP3 inflammasome enhances the proliferation and migration of A549 lung cancer cells

2016 ◽  
Vol 35 (4) ◽  
pp. 2053-2064 ◽  
Author(s):  
YANLI WANG ◽  
HUI KONG ◽  
XIAONING ZENG ◽  
WENRUI LIU ◽  
ZAILIANG WANG ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Nlrp3 Inflammasome ◽  
Lung Cancer Cells ◽  
And Migration ◽  
A549 Lung ◽  
Proliferation And Migration

scholarly journals Curcumin Inhibits Proliferation and Migration of A549 Lung Cancer Cells Through Activation of ERK1/2 Pathway-induced Autophagy

2019 ◽  
Vol 14 (6) ◽  
pp. 1934578X1984817
Author(s):  
Quangang Chen ◽  
Yanjuan Men ◽  
Hui Wang ◽  
Renjin Chen ◽  
Xufeng Han ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
And Migration ◽  
A549 Lung ◽  
Proliferation And Migration

Knockdown CYP2S1 inhibits lung cancer cells proliferation and migration

2021 ◽  
pp. 1-9
Author(s):  
Huan Guo ◽  
Baozhen Zeng ◽  
Liqiong Wang ◽  
Chunlei Ge ◽  
Xianglin Zuo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Lung Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

BACKGROUND: The incidence of lung cancer in Yunnan area ranks firstly in the world and underlying molecular mechanisms of lung cancer in Yunnan region are still unclear. We screened a novel potential oncogene CYP2S1 used mRNA microassay and bioinformation database. The function of CYP2S1 in lung cancer has not been reported. OBJECTIVE: To investigate the functions of CYP2S1 in lung cancer. METHODS: Immunohistochemistry and Real-time PCR were used to verify the expression of CYP2S1. Colony formation and Transwell assays were used to determine cell proliferation, invasion and migration. Xenograft assays were used to detected cell growth in vivo. RESULTS: CYP2S1 is significantly up-regulated in lung cancer tissues and cells. Knockdown CYP2S1 in lung cancer cells resulted in decrease cell proliferation, invasion and migration in vitro. Animal experiments showed downregulation of CYP2S1 inhibited lung cancer cell growth in vivo. GSEA analysis suggested that CYP2S1 played functions by regulating E2F targets and G2M checkpoint pathway which involved in cell cycle. Kaplan-Meier analysis indicated that patients with high CYP2S1 had markedly shorter event overall survival (OS) time. CONCLUSIONS: Our data demonstrate that CYP2S1 exerts tumor suppressor function in lung cancer. The high expression of CYP2S1 is an unfavorable prognostic marker for patient survival.

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