Loss of PDCD4 expression in human lung cancer correlates with tumour progression and prognosis

2003 ◽  
Vol 200 (5) ◽  
pp. 640-646 ◽  
Author(s):  
Yuan Chen ◽  
Thomas Knösel ◽  
Glen Kristiansen ◽  
Agnieszka Pietas ◽  
Mitchell E Garber ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Human Lung ◽  
Tumour Progression ◽  
Human Lung Cancer ◽  
Pdcd4 Expression

scholarly journals Allelic loss on chromosome 10q in human lung cancer: association with tumour progression and metastatic phenotype

1998 ◽  
Vol 77 (2) ◽  
pp. 270-276 ◽  
Author(s):  
S Petersen ◽  
G Wolf ◽  
U Bockmühl ◽  
K Gellert ◽  
M Dietel ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Human Lung ◽  
Tumour Progression ◽  
Human Lung Cancer ◽  
Allelic Loss ◽  
Metastatic Phenotype ◽  
Chromosome 10Q

scholarly journals Identification of a Clinically Relevant Signature for Early Progression in KRAS-Driven Lung Adenocarcinoma

2019 ◽  
Author(s):  
Sarah Neidler ◽  
Björn Kruspig ◽  
Kay Hewit ◽  
Tiziana Monteverde ◽  
Katarina Gyuraszova ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Overall Survival ◽  
Mouse Model ◽  
Lung Adenocarcinoma ◽  
Cancer Progression ◽  
Human Lung ◽  
Tumour Progression ◽  
Human Lung Cancer ◽  
Invasive Adenocarcinoma ◽  
Molecular Events

Inducible genetically defined mouse models of cancer uniquely facilitate the investigation of early events in cancer progression, however there are valid concerns about the ability of such models to faithfully recapitulate human disease.  We developed an inducible mouse model of progressive lung adenocarcinoma (LuAd) that combines sporadic activation of oncogenic KRasG12D with modest overexpression of c-MYC (KM model). Histological examination revealed a highly reproducible transition from adenoma to locally invasive adenocarcinoma within 6 weeks of oncogene activation.  Laser-capture microdissection coupled with RNA-SEQ was employed to determine transcriptional changes associated with tumour progression.  Upregulated genes were triaged for relevance to human LuAd using datasets from Oncomine and cBioportal.  Selected genes were validated by RNAi screening in human lung cancer cell lines and examined for association with lung cancer patient overall survival using KMplot.com.  Depletion of progression-associated genes resulted in pronounced viability and/or cell migration defects in human lung cancer cells.  Progression-associated genes moreover exhibited strong associations with overall survival, specifically in human lung adenocarcinoma, but not in squamous cell carcinoma. The KM mouse model faithfully recapitulates key molecular events in human lung cancer and is a useful tool for mechanistic interrogation of LuAd progression.

scholarly journals Identification of a Clinically Relevant Signature for Early Progression in KRAS-Driven Lung Adenocarcinoma

Cancers ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 600 ◽  
Author(s):  
Neidler ◽  
Kruspig ◽  
Hewit ◽  
Monteverde ◽  
Gyuraszova ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Overall Survival ◽  
Mouse Model ◽  
Lung Adenocarcinoma ◽  
Cancer Progression ◽  
Human Lung ◽  
Tumour Progression ◽  
Human Lung Cancer ◽  
Low Grade ◽  
Invasive Adenocarcinoma

Inducible genetically defined mouse models of cancer uniquely facilitate the investigation of early events in cancer progression, however, there are valid concerns about the ability of such models to faithfully recapitulate human disease. We developed an inducible mouse model of progressive lung adenocarcinoma (LuAd) that combines sporadic activation of oncogenic KRasG12D with modest overexpression of c-MYC (KM model). Histological examination revealed a highly reproducible spontaneous transition from low-grade adenocarcinoma to locally invasive adenocarcinoma within 6 weeks of oncogene activation. Laser-capture microdissection coupled with RNA-SEQ (ribonucleic acid sequencing) was employed to determine transcriptional changes associated with tumour progression. Upregulated genes were triaged for relevance to human LuAd using datasets from Oncomine and cBioportal. Selected genes were validated by RNAi screening in human lung cancer cell lines and examined for association with lung cancer patient overall survival using KMplot.com. Depletion of progression-associated genes resulted in pronounced viability and/or cell migration defects in human lung cancer cells. Progression-associated genes moreover exhibited strong associations with overall survival, specifically in human lung adenocarcinoma, but not in squamous cell carcinoma. The KM mouse model faithfully recapitulates key molecular events in human adenocarcinoma of the lung and is a useful tool for mechanistic interrogation of KRAS-driven LuAd progression.

scholarly journals Spatially discrete signalling niches regulate fibroblast heterogeneity in human lung cancer

2020 ◽  
Author(s):  
CJ Hanley ◽  
S Waise ◽  
R Parker ◽  
MA Lopez ◽  
J Taylor ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Human Lung ◽  
Phenotypic Diversity ◽  
Tumour Progression ◽  
Human Lung Cancer ◽  
Marker Genes ◽  
Valuable Insight ◽  
Fibroblast Activation ◽  
Fibroblast Heterogeneity ◽  
Tgf Β1

AbstractFibroblasts are functionally heterogeneous cells, capable of promoting and suppressing tumour progression. Across cancer types, the extent and cause of this phenotypic diversity remains unknown. We used single-cell RNA sequencing and multiplexed immunohistochemistry to examine fibroblast heterogeneity in human lung and non-small cell lung cancer (NSCLC) samples. This identified seven fibroblast subpopulations: including inflammatory fibroblasts and myofibroblasts (representing terminal differentiation states), quiescent fibroblasts, proto-myofibroblasts (x2) and proto-inflammatory fibroblasts (x2). Fibroblast subpopulations were variably distributed throughout tissues but accumulated at discrete niches associated with differentiation status. Bioinformatics analyses suggested TGF-β1 and IL-1 as key regulators of myofibroblastic and inflammatory differentiation respectively. However, in vitro analyses showed that whilst TGF-β1 stimulation in combination with increased tissue tension could induce myofibroblast marker expression, it failed to fully re-capitulate ex-vivo phenotypes. Similarly, IL-1β treatment only induced upregulation of a subset of inflammatory fibroblast marker genes. In silico modelling of ligand-receptor signalling identified additional pathways and cell interactions likely to be involved in fibroblast activation, which can be examined using publicly available R shiny applications (at the following links: myofibroblast activation and inflammatory fibroblast activation). This highlighted a potential role for IL-11 and IL-6 (among other ligands) in myofibroblast and inflammatory fibroblast activation respectively. This analysis provides valuable insight into fibroblast subtypes and differentiation mechanisms in NSCLC.

Ras Denitrosylation in Human Lung Cancer

2012 ◽  
Vol 3 (2) ◽  
pp. 135-139
Author(s):  
Benjamin Gaston ◽  
Nadzeya Marozkina
Keyword(s):  
Lung Cancer ◽  
Human Lung ◽  
Human Lung Cancer

MicroRNAs expression signature in human lung cancer cell

2014 ◽  
Author(s):  
Geyu Liang ◽  
Xikai Wang ◽  
Yanqiu Zhang ◽  
Yanyun Fu ◽  
Lihong Yin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cell ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Human Lung Cancer Cell ◽  
Expression Signature

Inhibitory effects of Actinidia Chinensis planch root extracts (acRoots) on human lung cancer cells through retinoic acid receptor beta

2017 ◽  
Vol 5 (1) ◽  
Author(s):  
Lingyan Wang ◽  
Jiayun Hou ◽  
Minghuan Zheng ◽  
Lin Shi
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Human Lung ◽  
Retinoic Acid Receptor ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Inhibitory Effects ◽  
The Core ◽  
Human Lung Cancer Cells ◽  
Receptor Beta

Actinidia Chinensis Planch roots (acRoots) are used to treat many cancers, although the anti-tumor mechanism by which acRoots inhibit cancer cell growth remains unclear. The present study aims at investigating inhibitory effects of acRoots on human lung cancer cells and potential mechanisms. Our data demonstrate that the inhibitory effects of acRoots on lung cancer cells depend on genetic backgrounds and phenotypes of cells. We furthermore found the expression of metabolism-associated gene profiles varied between acRoots-hypersensitive (H460) or hyposensitive lung cancer cells (H1299) after screening lung cancer cells with different genetic backgrounds. We selected retinoic acid receptor beta (RARB) as the core target within metabolism-associated core gene networks and evaluated RARB changes and roles in cells treated with acRoots at different concentrations and timeframes. Hypersensitive cancer cells with the deletion of RARB expression did not response to the treatment with acRoots, while RARB deletion did not change effects of acRoots on hyposensitive cells. Thus, it seems that RARB as the core target within metabolism-associated networks plays important roles in the regulation of lung cancer cell sensitivity to acRoots.

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