scholarly journals Effects of tanshinones mediated by forkhead box O3a transcription factor on the proliferation and apoptosis of lung cancer cells

2018 ◽  
Author(s):  
Dongjie� Liu ◽  
Renbing� Yuan ◽  
Fang� Yang ◽  
Dehui� Zhang
Keyword(s):  
Lung Cancer ◽  
Transcription Factor ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Forkhead Box ◽  
Proliferation And Apoptosis ◽  
Forkhead Box O3a

scholarly journals Upregulation of Complement Factor H by SOCS-1/3–STAT4 in Lung Cancer

Cancers ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 471 ◽  
Author(s):  
Yeon-Hee Yoon ◽  
Hyeon-Ji Hwang ◽  
Hye-Jin Sung ◽  
Sun-Hee Heo ◽  
Dong-Sun Kim ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Transcription Factor ◽  
Cancer Cells ◽  
Expression Patterns ◽  
Factor H ◽  
Complement Factor H ◽  
Lung Cancer Cells ◽  
Luciferase Reporter ◽  
Complement Factor ◽  
Low Level

Complement factor H (CFH) is a fluid phase regulator of complement proteins and functions to prevent complement attack and immune surveillance. CFH is known to inactivate therapeutic antibody-dependent complement-mediated cellular cytotoxicity. We found that CFH was highly expressed in human lung cancer cells and tissues. To investigate mechanisms of CFH upregulation, we searched for a CFH transcription factor and its regulatory factors. First, signal transducer and activator of transcription 4 (STAT4) expression patterns coincided with CFH expression patterns in lung cancer tissues. Knockdown of STAT4 led to decreased CFH secretion from lung cancer cells. STAT4 bound directly to the CFH promoter, as demonstrated by luciferase reporter assay, electrophoretic mobility shift assay (EMSA), and chromatin immunoprecipitation (ChIP) assay, suggesting that STAT4 is a transcription factor for CFH. In addition, a low level of suppressors of cytokine signaling (SOCS)-1/3, a Janus kinase (JAK) inhibitor, was observed in lung cancer cells and its transfection decreased CFH protein levels and promoter activity. Unexpectedly, the low level of SOCS-1/3 was not due to epigenetic silencing. Instead, differential methylation was found on the regulatory region of STAT4 between normal and lung cancer cells. In conclusion, our results demonstrated that CFH is upregulated by constitutive activation of STAT4, which is accounted for by SOCS silencing in lung cancer cells.

scholarly journals Effects and mechanism of downregulation of survivin expression by RNA interference on proliferation and apoptosis of lung cancer cells

2012 ◽  
Vol 5 (4) ◽  
pp. 917-922 ◽  
Author(s):  
XIANG-QI CHEN ◽  
SHENG YANG ◽  
ZHI-YING LI ◽  
HUI-SHAN LU ◽  
MING-QIANG KANG ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Rna Interference ◽  
Cancer Cells ◽  
Survivin Expression ◽  
Lung Cancer Cells ◽  
Proliferation And Apoptosis

scholarly journals Protective Effect of Caffeic Acid on Paclitaxel Induced Anti-Proliferation and Apoptosis of Lung Cancer Cells Involves NF-κB Pathway

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 ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Protective Effect ◽  
Cancer Cells ◽  
Caffeic Acid ◽  
Lung Cancer Cells ◽  
Proliferation And Apoptosis

scholarly journals Inhibition of ITCH Suppresses Proliferation and Induces Apoptosis of Lung Cancer Cells

2018 ◽  
Vol 48 (4) ◽  
pp. 1703-1709 ◽  
Author(s):  
Peng-Fei Li ◽  
Qi-Gang Zhang
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Cancer Proliferation ◽  
Flow Cytometric ◽  
Tumor Tissues ◽  
Proliferation And Apoptosis ◽  
Underlying Mechanisms ◽  
Cancer Tissues ◽  
Proliferation And Invasion

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.

scholarly journals Function of miR-200a in proliferation and apoptosis of non-small cell lung cancer cells

2020 ◽  
Vol 20 (2) ◽  
pp. 1256-1262
Author(s):  
Yan Huang ◽  
Ting Bao ◽  
Zhenzhen Li ◽  
Guiyi Ji ◽  
Li Zhang
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Small Cell Lung ◽  
Proliferation And Apoptosis

scholarly journals Long Noncoding RNA PTPRG Antisense RNA 1 Reduces Radiosensitivity of Nonsmall Cell Lung Cancer Cells Via Regulating MiR-200c-3p/TCF4

2020 ◽  
Vol 19 ◽  
pp. 153303382094261
Author(s):  
Qiang Ma ◽  
Rungui Niu ◽  
Wei Huang ◽  
Liangshan Da ◽  
Yanlei Tang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Transcription Factor ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Antisense Rna ◽  
Nonsmall Cell Lung Cancer ◽  
Lung Cancer Cells ◽  
X Ray ◽  
Transcription Factor 4 ◽  
Cancer Tissues

Background: PTPRG antisense RNA 1 has been well-documented to exert an oncogenic role in diverse neoplasms. However, the precise role of PTPRG antisense RNA 1 in regulating radiosensitivity of nonsmall cell lung cancer cells remains largely elusive. Methods: Expression levels of PTPRG antisense RNA 1 and miR-200c-3p in nonsmall cell lung cancer tissues and cells were detected by quantitative real-time polymerase chain reaction, while transcription factor 4 expression was examined by immunohistochemistry and Western blot. After nonsmall cell lung cancer cells were exposed to X-ray with different doses in vitro, Cell Counting Kit -8 assay and colony formation assay were conducted to determine the influence of PTPRG antisense RNA 1 on cell viability. Interaction between miR-200c-3p and PTPRG antisense RNA 1 as well as transcription factor 4 was investigated by dual luciferase reporter assay. Result: In nonsmall cell lung cancer tissues, the expressions of PTPRG antisense RNA 1 and transcription factor 4 were significantly upregulated, whereas the expression of miR-200c-3p was downregulated. It was also proved that PTPRG antisense RNA 1 and 3′-untranslated region of transcription factor 4 can bind to miR-200c-3p. Under X-ray irradiation, overexpressed PTPRG antisense RNA 1 could promote the viability and enhance the radioresistance of nonsmall cell lung cancer cells, and this effect was partially weakened by miR-200c-3p mimics. Transcription factor 4 was identified as a target gene of miR-200c-3p, which could be positively regulated by PTPRG antisense RNA 1. Conclusion: PTPRG antisense RNA 1 reduces the radiosensitivity of nonsmall cell lung cancer cells via modulating miR-200c-3p/TCF4 axis.

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 ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Proliferation And Apoptosis
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