Abstract 3738: IL-24 modulates the high mobility group (HMG) A1/miR222 /AKT signaling in lung cancer cells

2016 ◽  
Author(s):  
Janani Panneerselvam ◽  
Akhil Srivastava ◽  
Ranganayaki Muralidharan ◽  
Qi Wang ◽  
Wei Zheng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
High Mobility ◽  
Akt Signaling ◽  
High Mobility Group ◽  
Lung Cancer Cells

scholarly journals IL-24 modulates the high mobility group (HMG) A1/miR222 /AKT signaling in lung cancer cells

Oncotarget ◽  
2016 ◽  
Vol 7 (43) ◽  
pp. 70247-70263 ◽  
Author(s):  
Janani Panneerselvam ◽  
Akhil Srivastava ◽  
Ranganayaki Muralidharan ◽  
Qi Wang ◽  
Wei Zheng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
High Mobility ◽  
Akt Signaling ◽  
High Mobility Group ◽  
Lung Cancer Cells

scholarly journals Enhancement of Cisplatin Sensitivity in High Mobility Group 2 cDNA-transfected Human Lung Cancer Cells

1999 ◽  
Vol 90 (1) ◽  
pp. 108-115 ◽  
Author(s):  
Hitoshi Arioka ◽  
Kazuto Nishio ◽  
Tomoyuki Ishida ◽  
Hisaoh Fukumoto ◽  
Kazuya Fukuoka ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Human Lung ◽  
High Mobility ◽  
High Mobility Group ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Human Lung Cancer Cells ◽  
Cisplatin Sensitivity ◽  
Group 2

High-mobility group A1 proteins enhance the expression of the oncogenic miR-222 in lung cancer cells

2011 ◽  
Vol 357 (1-2) ◽  
pp. 363-371 ◽  
Author(s):  
Yunzhi Zhang ◽  
Teng Ma ◽  
Shuping Yang ◽  
Mingying Xia ◽  
Jing Xu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
High Mobility ◽  
High Mobility Group ◽  
Lung Cancer Cells

scholarly journals PRMT5 Promotes EMT Through Regulating Akt Activity in Human Lung Cancer

2021 ◽  
Vol 30 ◽  
pp. 096368972110017
Author(s):  
Jianhao Huang ◽  
Yonghua Zheng ◽  
Xiao Zheng ◽  
Bao Qian ◽  
Qi Yin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Human Lung ◽  
Akt Signaling ◽  
Lung Cancer Cells ◽  
Signaling Cascades ◽  
Human Lung Cancer ◽  
Mesenchymal Transition ◽  
Human Lung Cancer Cells

The type II protein arginine methyltransferase 5 (PRMT5) has been engaged in various human cancer development and progression types. Nevertheless, few studies uncover the biological functions of PRMT5 in the epithelial-mesenchymal transition (EMT) of human lung cancer cells, and the associated molecular mechanisms and signaling cascades are entirely unknown. Here, we show that PRMT5 is the ectopic expression in human lung cancer tissues and cell lines. Further study reveals that silencing PRMT5 by lentivirus-mediated shRNA or blocking of PRMT5 by specific inhibitor GSK591 attenuates the expression levels of EMT-related markers in vivo, using the xenograft mouse model. Moreover, our results show that down-regulation of PRMT5 impairs EGFR/Akt signaling cascades in human lung cancer cells, whereas re-expression of PRMT5 recovers those changes, suggesting that PRMT5 regulates EMT probably through EGFR/Akt signaling axis. Altogether, our results demonstrate that PRMT5 serves as a critical oncogenic regulator and promotes EMT in human lung cancer cells. More importantly, our findings also suggest that PRMT5 may be a potential therapeutic candidate for the treatment of human lung cancer.

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