scholarly journals Hypoxia-inducible factor-1? in non small cell lung cancer: Relation to growth factor, protease and apoptosis pathways

2004 ◽  
Vol 111 (1) ◽  
pp. 43-50 ◽  
Author(s):  
Daniel E.B. Swinson ◽  
J. Louise Jones ◽  
Giles Cox ◽  
Donna Richardson ◽  
Adrian L. Harris ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Growth Factor ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Hypoxia Inducible Factor ◽  
Small Cell ◽  
Small Cell Lung ◽  
Hypoxia Inducible Factor 1 ◽  
Apoptosis Pathways

DEC1 (STRA13) protein expression relates to hypoxia- inducible factor 1-alpha and carbonic anhydrase-9 overexpression in non-small cell lung cancer

2003 ◽  
Vol 200 (2) ◽  
pp. 222-228 ◽  
Author(s):  
Alexandra Giatromanolaki ◽  
Michael I Koukourakis ◽  
Efthimios Sivridis ◽  
Helen Turley ◽  
Charles C Wykoff ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Carbonic Anhydrase ◽  
Protein Expression ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Hypoxia Inducible Factor ◽  
Small Cell ◽  
Small Cell Lung ◽  
Hypoxia Inducible Factor 1 ◽  
Carbonic Anhydrase 9

scholarly journals Independent Prognostic Value of Hypoxia-inducible Factor 1-alpha Expression in Small Cell Lung Cancer

2017 ◽  
Vol 14 (8) ◽  
pp. 785-790 ◽  
Author(s):  
Chang-Sheng Lin ◽  
Tu-Chen Liu ◽  
Ming-Tsung Lee ◽  
Shun-Fa Yang ◽  
Thomas Chang-Yao Tsao
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Prognostic Value ◽  
Hypoxia Inducible Factor ◽  
Small Cell ◽  
Small Cell Lung ◽  
Hypoxia Inducible Factor 1

P-489 Hypoxia inducible factor-1 alpha in non-small cell lung cancer: Relation to other biological factors and prognosis

Lung Cancer ◽  
2003 ◽  
Vol 41 ◽  
pp. S214
Author(s):  
Daniel E.B. Swinson ◽  
J. Louise Jones ◽  
Giles Cox ◽  
Donna Richardson ◽  
Adrian Harris ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Hypoxia Inducible Factor ◽  
Small Cell ◽  
Biological Factors ◽  
Small Cell Lung ◽  
Hypoxia Inducible Factor 1

scholarly journals Silibinin Regulates Tumor Progression and Tumorsphere Formation by Suppressing PD-L1 Expression in Non-Small Cell Lung Cancer (NSCLC) Cells

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1632
Author(s):  
Alexis Rugamba ◽  
Dong Young Kang ◽  
Nipin Sp ◽  
Eun Seong Jo ◽  
Jin-Moo Lee ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Growth Factor ◽  
Small Cell Lung Cancer ◽  
Anticancer Activity ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Molecular Signaling ◽  
Small Cell Lung

Recently, natural compounds have been used globally for cancer treatment studies. Silibinin is a natural compound extracted from Silybum marianum (milk thistle), which has been suggested as an anticancer drug through various studies. Studies on its activity in various cancers are undergoing. This study demonstrated the molecular signaling behind the anticancer activity of silibinin in non-small cell lung cancer (NSCLC). Quantitative real-time polymerase chain reaction and Western blotting analysis were performed for molecular signaling analysis. Wound healing assay, invasion assay, and in vitro angiogenesis were performed for the anticancer activity of silibinin. The results indicated that silibinin inhibited A549, H292, and H460 cell proliferation in a concentration-dependent manner, as confirmed by the induction of G0/G1 cell cycle arrest and apoptosis and the inhibition of tumor angiogenesis, migration, and invasion. This study also assessed the role of silibinin in suppressing tumorsphere formation using the tumorsphere formation assay. By binding to the epidermal growth factor receptor (EGFR), silibinin downregulated phosphorylated EGFR expression, which then inhibited its downstream targets, the JAK2/STAT5 and PI3K/AKT pathways, and thereby reduced matrix metalloproteinase, PD-L1, and vascular endothelial growth factor expression. Binding analysis demonstrated that STAT5 binds to the PD-L1 promoter region in the nucleus and silibinin inhibited the STAT5/PD-L1 complex. Altogether, silibinin could be considered as a candidate for tumor immunotherapy and cancer stem cell-targeted therapy.

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