scholarly journals Nucleobindin-2 mRNA level is down regulated in KRAS-mutation lung cancer cell lines compared with EGFR/BRAF/KRAS wild-type lung cancer cell lines

2019 ◽  
Vol 3 (1) ◽  
Author(s):  
Sunaga Noriaki ◽  
Imai Hisao ◽  
Okada Junichi ◽  
Yamada Eijiro ◽  
Okada Shuichi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Kras Mutation ◽  
Mrna Level ◽  
Cancer Cell Lines ◽  
Wild Type ◽  
Lung Cancer Cell

scholarly journals Nucleobindin-2 mRNA level is down regulated in KRAS-mutation lung cancer cell lines compared with EGFR/BRAF/KRAS wild-type lung cancer cell lines

2019 ◽  
Vol 3 (1) ◽  
Author(s):  
Sunaga Noriaki ◽  
Imai Hisao ◽  
Okada Junichi ◽  
Yamada Eijiro ◽  
Okada Shuichi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Kras Mutation ◽  
Mrna Level ◽  
Cancer Cell Lines ◽  
Wild Type ◽  
Lung Cancer Cell

scholarly journals MiR-9-1 Suppresses Cell Proliferation and Promotes Apoptosis by Targeting UHRF1 in Lung Cancer

2021 ◽  
Vol 20 ◽  
pp. 153303382110411
Author(s):  
Cheng-You Jia ◽  
Wei Xiang ◽  
Ji-Bin Liu ◽  
Geng-Xi Jiang ◽  
Feng Sun ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cancer Cell ◽  
Mrna Level ◽  
A549 Cells ◽  
Cancer Cell Lines ◽  
G1 Arrest ◽  
Lung Cancer Cell

Lung cancer is listed as the most common reason for cancer-related death all over the world despite diagnostic improvements and the development of chemotherapy and targeted therapies. MicroRNAs control both physiological and pathological processes including development and cancer. A microRNA-9 to 1 (miR-9 to 1) overexpression model in lung cancer cell lines was established and miR-9 to 1 was found to significantly suppress the proliferation rate in lung cancer cell lines, colony formation in vitro, and tumorigenicity in nude mice of A549 cells. Ubiquitin-like containing PHD and RING finger domains 1 (UHRF1) was then identified to direct target of miR-9 to 1. The inhibition of UHRF1 by miR-9 to 1 causes G1 arrest and p15, p16, and p21 were re-expressed in miR-9 to 1 group in mRNA level and protein level. Silence of UHRF1 expression in A549 cells resulted in the similar re-expression of p15, p16, p21 which is similar with miR-9 to 1 infection. Therefore, we concluded that UHRF1 is a new target for miR-9 to 1 to suppress cell proliferation by re-expression of tumor suppressors p15, p16, and p21 mediated by UHRF1.

IRX4204 in combination with erlotinib to target distinct pathways in lung cancer cells.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e14095-e14095 ◽  
Author(s):  
Xi Liu ◽  
Jason Roszik ◽  
Masanori Karakami ◽  
Martin Sanders ◽  
Rosh Chandraratna ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Line ◽  
Cell Lines ◽  
Cancer Cell ◽  
Mrna Level ◽  
Cancer Cell Lines ◽  
Clinical Activity ◽  
Lung Cancer Cell ◽  
Ampk Signaling ◽  
Phosphorylated Akt

e14095 Background: IRX4204 is a Retinoid X Receptor (RXR) specific agonist (rexinoid). IRX4204 has high potency as a RXR agonist with low binding affinity to Retinoic Acid Receptors (RARs), PPAR, FXR or LXR. Our prior work with the less specific rexinoid bexarotene and erlotinib showed clinical activity in patients with lung cancer cases that harbored KRAS mutations. IRX4204 inhibits lung cancer cell proliferation and can chemoprevent carcinogen-induced lung cancers in mice. We sought to explore the underlying mechanisms engaged by the combination of IRX4204 and erlotinib. Materials and Methods: Human (H1703 and HOP62) and murine (ED1 and LKR13) lung cancer cell lines were treated with IRX4204, erlotinib, IRX4204 plus erlotinib, or vehicle. Reverse phase protein array (RPPA) and mRNA microarray analyses were performed to analyze comprehensively for differentially expressed growth regulatory proteins. Results: Combination of IRX4204 and erlotinib suppressed proliferation of both KRAS mutant (HOP62 and LKR13) and wild-type (H1703 and ED1) lung cancer cell lines. Additive effect was observed as compared to IRX4204 or erlotinib treatment alone. Combining IRX4204 with erlotinib markedly increased inhibition of specific therapeutic targets including Src, phosphorylated Akt and ribosomal S6 proteins. At the mRNA level, Ingenuity Pathway Analysis of species significantly increased or decreased by the combination treatment revealed multiple pathways related to oncogenic signaling. Specifically, we found in H1703 cell line regulation of Granzyme A and AMPK signaling and in HOP62 cell line inhibition of angiogenesis was implicated by altering TSP1 expression. Notably, in ED1 cell line PPARα/RXRα activation, PTEN signaling, PI3K/AKT signaling, TGF-β signaling, and AMPK signaling were each associated with effects of IRX4204 combined with erlotinib. Conclusions: Taken together, these data highlight specific mechanisms and candidate pharmacodynamic biomarkers of response to the combination of this rexinoid and EGFR-TKI in lung cancer. Based on these findings, a clinical trial (NCT02991651) with IRX4204 in combination with erlotinib is underway to treat patients with chemotherapy-refractory non-small cell lung cancer.

P12.04 Radiation Mediates IDO1 Dynamic Changes in KRAS Mutation Lung Cancer Cell Lines

2021 ◽  
Vol 16 (10) ◽  
pp. S1008
Author(s):  
Y. Lan ◽  
W. Pi ◽  
X. Xia ◽  
W. Wang ◽  
Z. Zhou ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Kras Mutation ◽  
Cancer Cell Lines ◽  
Lung Cancer Cell ◽  
Dynamic Changes

scholarly journals Expression profiling of lung cancer cell lines

10.1038/87074 ◽  
2001 ◽  
Vol 27 (S4) ◽  
pp. 53-53
Author(s):  
Priya Dayananth ◽  
Terri McClanahan ◽  
Ferdous Gheyas ◽  
Marco Hernandez ◽  
Wei Ding ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Expression Profiling ◽  
Cancer Cell Lines ◽  
Lung Cancer Cell

scholarly journals Failure of apoptosis and activation on NFκB by celecoxib and aspirin in lung cancer cell lines

2007 ◽  
Author(s):  
Angela Gradilone ◽  
Ida Silvestri ◽  
Susanna Scarpa ◽  
Stefania Morrone ◽  
Orietta Gandini ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Lung Cancer Cell
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