scholarly journals Effects of mdig on proliferation and apoptosis of lung cancer cells

2018 ◽  
Author(s):  
Xiaohui Xu ◽  
Lei Cao ◽  
Ye Zhang ◽  
Hongjian Lian ◽  
Zhiwei Sun ◽  
...  
2012 ◽  
Vol 5 (4) ◽  
pp. 917-922 ◽  
Author(s):  
XIANG-QI CHEN ◽  
SHENG YANG ◽  
ZHI-YING LI ◽  
HUI-SHAN LU ◽  
MING-QIANG KANG ◽  
...  

2012 ◽  
Vol 13 (5) ◽  
pp. 6236-6245 ◽  
Author(s):  
Chien-Liang Lin ◽  
Ruei-Feng Chen ◽  
Jeff Yi-Fu Chen ◽  
Ying-Chieh Chu ◽  
Hui-Min Wang ◽  
...  

2018 ◽  
Vol 48 (4) ◽  
pp. 1703-1709 ◽  
Author(s):  
Peng-Fei Li ◽  
Qi-Gang Zhang

Background/Aims: The E3 ubiquitin ligase ITCH plays an important role in invasive and metastatic cancers. However, the role of ITCH in the progression of lung cancer has not been fully described. Methods: Real-time PCR was used to detect the expression of ITCH mRNA in the tumor tissues and paracarcinoma tissues from 32 patients with lung cancer. SiRNA was used to inhibit the expression of ITCH in two lung cancer cell lines, H1975 and Calu3 and the cell proliferation and apoptosis were measured by MTT and flow cytometric assay. In addition, to further investigate whether ITCH affected the apoptosis of cancer cells and its underlying mechanisms, the expression of important markers of apoptosis and invasion in lung cancer cells were detected by Western blot. Results: The study showed significant increments in the expression of ITCH in lung cancer tissues (p< 0.001). ITCH siRNA effectively inhibited the proliferation and invasion of the lung cancer cells and promoted cell apoptosis. Molecular analysis further showed significant reductions in the expression of Bcl2, MMP2, MMP9 and β-catenin and an increase in the expression of Bax and E-cadherin in the lung cancer cells with ITCH deficiency. Conclusions: Inhibition of ITCH might suppress lung cancer proliferation and invasion via regulation of MMPs, EMT and Bcl2/Bax signaling pathway.


2020 ◽  
Vol 20 (2) ◽  
pp. 1256-1262
Author(s):  
Yan Huang ◽  
Ting Bao ◽  
Zhenzhen Li ◽  
Guiyi Ji ◽  
Li Zhang

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Mark E. Reeves ◽  
Matthew Firek ◽  
Shin-Tai Chen ◽  
Yousef Amaar

RASSF1A has been demonstrated to be a tumor suppressor, while RASSF1C is now emerging as a growth promoting protein in breast and lung cancer cells. To further highlight the dual functionality of the RASSF1 gene, we have compared the effects of RASSF1A and RASSF1C on cell proliferation and apoptosis in the presence of TNF-α. Overexpression of RASSF1C in breast and lung cancer cells reduced the effects of TNF-α on cell proliferation, apoptosis, and MST1/2 phosphorylation, while overexpression of RASSF1A had the opposite effect. We also assessed the expression of RASSF1A and RASSF1C in breast and lung tumor and matched normal tissues. We found that RASSF1A mRNA levels are significantly higher than RASSF1C mRNA levels in all normal breast and lung tissues examined. In addition, RASSF1A expression is significantly downregulated in 92% of breast tumors and in 53% of lung tumors. Conversely, RASSF1C was upregulated in 62% of breast tumors and in 47% of lung tumors. Together, these findings suggest that RASSF1C, unlike RASSF1A, is not a tumor suppressor but instead may play a role in stimulating survival in breast and lung cancer cells.


Sign in / Sign up

Export Citation Format

Share Document