scholarly journals Immunoglobulin-like transcript 4 promotes tumor progression and metastasis and up-regulates VEGF-C expression via ERK signaling pathway in non-small cell lung cancer

Oncotarget ◽  
2015 ◽  
Vol 6 (15) ◽  
pp. 13550-13563 ◽  
Author(s):  
Pei Zhang ◽  
Xiaosun Guo ◽  
Juan Li ◽  
Shuwen Yu ◽  
Linlin Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Tumor Progression ◽  
Signaling Pathway ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Erk Signaling ◽  
Small Cell Lung

scholarly journals Exploration in the mechanism of fucosterol for the treatment of non-small cell lung cancer based on network pharmacology and molecular docking

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xiaoling Li ◽  
Baixin Lin ◽  
Zhiping Lin ◽  
Yucui Ma ◽  
Qu Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Molecular Docking ◽  
Small Cell Lung Cancer ◽  
Signaling Pathway ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Erk Signaling ◽  
Network Pharmacology ◽  
Protein Interaction Data ◽  
Small Cell Lung

AbstractFucosterol, a sterol isolated from brown algae, has been demonstrated to have anti-cancer properties. However, the effects and underlying molecular mechanism of fucosterol on non-small cell lung cancer remain to be elucidated. In this study, the corresponding targets of fucosterol were obtained from PharmMapper, and NSCLC related targets were gathered from the GeneCards database, and the candidate targets of fucosterol-treated NSCLC were predicted. The mechanism of fucosterol against NSCLC was identified in DAVID6.8 by enrichment analysis of GO and KEGG, and protein–protein interaction data were collected from STRING database. The hub gene GRB2 was further screened out and verified by molecular docking. Moreover, the relationship of GRB2 expression and immune infiltrates were analyzed by the TIMER database. The results of network pharmacology suggest that fucosterol acts against candidate targets, such as MAPK1, EGFR, GRB2, IGF2, MAPK8, and SRC, which regulate biological processes including negative regulation of the apoptotic process, peptidyl-tyrosine phosphorylation, positive regulation of cell proliferation. The Raf/MEK/ERK signaling pathway initiated by GRB2 showed to be significant in treating NSCLC. In conclusion, our study indicates that fucosterol may suppress NSCLC progression by targeting GRB2 activated the Raf/MEK/ERK signaling pathway, which laying a theoretical foundation for further research and providing scientific support for the development of new drugs.

scholarly journals CD73 Is Regulated by the EGFR-ERK Signaling Pathway in Non-small Cell Lung Cancer

2021 ◽  
Vol 41 (3) ◽  
pp. 1231-1242
Author(s):  
SEBASTIAN GRIESING ◽  
BIN-CHI LIAO ◽  
JAMES CHIH-HSIN YANG
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Signaling Pathway ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Erk Signaling ◽  
Small Cell Lung

scholarly journals MEK inhibitors for the treatment of non-small cell lung cancer

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Jing Han ◽  
Yang Liu ◽  
Sen Yang ◽  
Xuan Wu ◽  
Hongle Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Signaling Pathway ◽  
Cell Lung Cancer ◽  
Mapk Signaling ◽  
Small Cell ◽  
Erk Signaling ◽  
Therapeutic Effects ◽  
Small Cell Lung ◽  
Mek Inhibitors

AbstractBRAF and KRAS are two key oncogenes in the RAS/RAF/MEK/MAPK signaling pathway. Concomitant mutations in both KRAS and BRAF genes have been identified in non-small cell lung cancer (NSCLC). They lead to the proliferation, differentiation, and apoptosis of tumor cells by activating the RAS/RAF/MEK/ERK signaling pathway. To date, agents that target RAS/RAF/MEK/ERK signaling pathway have been investigated in NSCLC patients harboring BRAF mutations. BRAF and MEK inhibitors have gained approval for the treatment of patients with NSCLC. According to the reported findings, the combination of MEK inhibitors with chemotherapy, immune checkpoint inhibitors, epidermal growth factor receptor-tyrosine kinase inhibitors or BRAF inhibitors is highly significant for improving clinical efficacy and causing delay in the occurrence of drug resistance. This review summarized the existing experimental results and presented ongoing clinical studies as well. However, further researches need to be conducted to indicate how we can combine other drugs with MEK inhibitors to significantly increase therapeutic effects on patients with lung cancer.

scholarly journals PGK1 Promotes NSCLC Progression by Enhancing Aerobic Glycolysis and Activating AKT/ERK Signaling Pathway

2021 ◽  
Author(s):  
Yongqin Tang ◽  
Mei Li ◽  
Jinxuan Hei ◽  
Likun Ma ◽  
Jianyuan Pan
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Signaling Pathway ◽  
Cell Lung Cancer ◽  
Aerobic Glycolysis ◽  
Small Cell ◽  
Erk Signaling ◽  
Cancer Development ◽  
Small Cell Lung ◽  
Glycolysis Pathway

Abstract Metabolic reprogramming, especially aerobic glycolysis is considered a hallmark of cancer, and is becoming a novel target for cancer therapy. Phosphoglycerate kinase I (PGK1) which is an important enzyme generating the first ATP in glycolysis pathway was already shown can promote some types of cancer development and progression, however, the role of PGK1 in lung cancer development is less reported. The aim of this study was to explore the mechanism of PGK1 in promoting non-small cell lung cancer (NSCLC) development and progression. Gene overexpression or silencing, scratch assay, Trans-well assay, western blot, immunohistochemistry, chromatin immunoprecipitation, real-time quantitative RT-PCR, MTT cell viability assay and mouse xenograft, glucose uptake, lactate secretion, ATP production and Extracellular Acidification Rate (ECAR) seahorse assay were performed to investigate the biological function and the underlying mechanism of PGK1 in NSCLC development. Our study found that PGK1 was high expressed in non-small cell lung cancer tissues, its expression is positive correlated with tumor grade and clinical stage and negative correlated with patients’ overall survival. Importantly, its expression was also associated with clinicopathological characteristics of lung cancer patients. Overexpression PGK1 could not only promote lung epithelial cell and tumor cell migration and proliferation in vitro, but also increase the tumor growth in vivo. Mechanically, PGK1 promotes NSCLC development and progression by activating AKT/ERK signaling pathway and altering aerobic glycolysis pathway. Meanwhile PGK1 was HIF1α downstream target gene and played an essential role in hypoxia-induced shift of glycolysis. In addition, the PGK1 expression was positive correlated with HIF1α expression in NSCLC tissues. Therefore, we concluded that PGK1 could be a biomarker for NSCLC diagnosis and outcome evaluation, and targeting PGK1 should be an innovative strategy for NSCLC therapy in the future.

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