Fisetin induces apoptosis and endoplasmic reticulum stress in human non-small cell lung cancer through inhibition of the MAPK signaling pathway

Tumor Biology ◽  
2016 ◽  
Vol 37 (7) ◽  
pp. 9615-9624 ◽  
Author(s):  
Kyoung Ah Kang ◽  
Mei Jing Piao ◽  
Susara Ruwan Kumara Madduma Hewage ◽  
Yea Seong Ryu ◽  
Min Chang Oh ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Small Cell Lung Cancer ◽  
Signaling Pathway ◽  
Cell Lung Cancer ◽  
Mapk Signaling ◽  
Small Cell ◽  
Mapk Signaling Pathway ◽  
Small Cell Lung

scholarly journals Rosmarinic acid reverses non‐small cell lung cancer cisplatin resistance by activating the MAPK signaling pathway

2020 ◽  
Vol 34 (5) ◽  
pp. 1142-1153 ◽  
Author(s):  
Xiao‐Zhong Liao ◽  
Ying Gao ◽  
Ling‐Ling Sun ◽  
Jia‐Hui Liu ◽  
Han‐Rui Chen ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Signaling Pathway ◽  
Cell Lung Cancer ◽  
Rosmarinic Acid ◽  
Cisplatin Resistance ◽  
Mapk Signaling ◽  
Small Cell ◽  
Mapk Signaling Pathway ◽  
Small Cell Lung

TRIM45 Suppresses the Development of Non-small Cell Lung Cancer

2020 ◽  
Vol 20 (4) ◽  
pp. 299-306
Author(s):  
Xiyang Peng ◽  
Yao Wen ◽  
Lagabaiyila Zha ◽  
Jian Zhuang ◽  
Li Lin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Cell Lung Cancer ◽  
Mapk Signaling ◽  
Small Cell ◽  
Mapk Signaling Pathway ◽  
Lung Cancer Cells ◽  
Small Cell Lung

Background: Previously, we first identified the human tripartite motifcontaining protein 45 (TRIM45) acts as a novel transcriptional repressor in mitogenactivated protein kinase (MAPK) signaling pathway. After that, the inhibitory role of TRIM45 in the development of tumor was gradually unveiled. However, the function of TRIM45 in the tumorigenesis of lung cancer has not been characterized. Methods and Results: In this study, we found that TRIM45 was up-regulated in earlystage human non-small-cell lung cancer (NSCLC) tissues. Overexpression of TRIM45 in lung cancer cells induces G1 arrest and promotes apoptosis, which accompanied by upregulated expression of RB, p16, p53, p27Kip1, and Caspase3 and down-regulated expression of CyclinE1 and CyclinE2. Further detection of the expression of the molecules in the MAPK signaling pathway revealed that overexpression of TRIM45 in lung cancer cells promotes phosphorylated p38 (p-p38) activation and inhibits phosphorylated ERK (p-ERK) activation. In accordance with this, p-p38 is increased while p-ERK is decreased in lung cancer tissues. Conclusion: These findings indicate that TRIM45 plays an inhibitory role in the tumorigenesis of lung cancer. High-level expression of TRIM45 in lung cancer tissue may promote cell apoptosis by activating p38 signal and inhibit proliferation by down-regulating p-ERK, which provides a new clue for understanding the tumorigenesis of lung cancer.

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