scholarly journals Tumor growth affects the metabonomic phenotypes of multiple mouse non-involved organs in an A549 lung cancer xenograft model

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Shan Xu ◽  
Yuan Tian ◽  
Yili Hu ◽  
Nijia Zhang ◽  
Sheng Hu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Growth ◽  
Xenograft Model ◽  
A549 Lung

scholarly journals LOXL1 Is Regulated by Integrin α11 and Promotes Non-Small Cell Lung Cancer Tumorigenicity

Cancers ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 705 ◽  
Author(s):  
Cédric Zeltz ◽  
Elena Pasko ◽  
Thomas R. Cox ◽  
Roya Navab ◽  
Ming-Sound Tsao
Keyword(s):  
Lung Cancer ◽  
Tumor Growth ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Xenograft Model ◽  
Tumor Stroma ◽  
Small Cell ◽  
Matrix Remodeling ◽  
Small Cell Lung

Integrin α11, a stromal collagen receptor, promotes tumor growth and metastasis of non-small cell lung cancer (NSCLC) and is associated with the regulation of collagen stiffness in the tumor stroma. We have previously reported that lysyl oxidase like-1 (LOXL1), a matrix cross-linking enzyme, is down-regulated in integrin α11-deficient mice. In the present study, we investigated the relationship between LOXL1 and integrin α11, and the role of LOXL1 in NSCLC tumorigenicity. Our results show that the expression of LOXL1 and integrin α11 was correlated in three lung adenocarcinoma patient datasets and that integrin α11 indeed regulated LOXL1 expression in stromal cells. Using cancer-associated fibroblast (CAF) with either a knockdown or overexpression of LOXL1, we demonstrated a role for LOXL1 in collagen matrix remodeling and collagen fiber alignment in vitro and in vivo in a NSCLC xenograft model. As a consequence of collagen reorganization in NSCLC tumor stroma, we showed that LOXL1 supported tumor growth and progression. Our findings demonstrate that stromal LOXL1, under regulation of integrin α11, is a determinant factor of NSCLC tumorigenesis and may be an interesting target in this disease.

scholarly journals Effects of Epigallocatechin-3-gallate (EGCG) on A549 Lung Cancer Tumor Growth and Angiogenesis

2013 ◽  
Vol 77 (9) ◽  
pp. 1799-1803 ◽  
Author(s):  
Yuhi SAKAMOTO ◽  
Nobuhiro TERASHITA ◽  
Takashi MURAGUCHI ◽  
Toshio FUKUSATO ◽  
Shunichiro KUBOTA
Keyword(s):  
Lung Cancer ◽  
Tumor Growth ◽  
Cancer Tumor ◽  
A549 Lung

Towards Personalized Medicine: Photoacoustic Imaging Enables Companion Diagnosis and Targeted Treatment of Lung Cancer

2020 ◽  
Author(s):  
Melissa Lucero ◽  
Jefferson Chan
Keyword(s):  
Lung Cancer ◽  
Personalized Medicine ◽  
Photoacoustic Imaging ◽  
Xenograft Model ◽  
Companion Diagnostics ◽  
Inhibit Tumor Growth ◽  
Improve Treatment ◽  
New Frontier ◽  
Time Changes ◽  
A549 Lung

<p>Companion diagnostics (CDx) represent a new frontier in personalized medicine that promises to improve treatment outcomes by matching therapies to patients. Currently, these tests are limited in scope and cannot report on real-time changes associated with disease progression and remediation. To address this, we have developed the first photoacoustic imaging-based CDx (PACDx) for the selective detection of elevated glutathione (GSH) in lung cancer. Since GSH is abundant in most cells, it was essential to tune the reactivity of the benzenesulfonyl-based trigger to distinguish between normal and pathological states. Moreover, we designed a matching prodrug, PARx, that utilizes the same mechanism to release both a chemotherapeutic (Gemcitabine) and a PA readout. We demonstrate that PARx can inhibit tumor growth while sparing all other tissue from off target toxicity in a A549 lung cancer xenograft model. We envision that this work will establish a new standard for personalized medicine by employing a unique imaging-based approach.</p>

Effects of Intermittent Cisplatin Intervention on 6PGD Levels and Tumor Growth and Migration in A549 Lung Cancer Cells

2021 ◽  
Vol 8 ◽  
Author(s):  
WU Qiang ◽  
TANG Lin-dong ◽  
WU Yan-hui ◽  
LI Qiang ◽  
YU Li
Keyword(s):  
Lung Cancer ◽  
Tumor Growth ◽  
Western Blot ◽  
Cancer Cells ◽  
A549 Cells ◽  
Lung Cancer Cells ◽  
Migration Ability ◽  
Western Blot Method ◽  
And Migration ◽  
A549 Lung

Aim: To investigate the changes of A549 protein 6PGD expression, tumor growth and migration, NADPH and ROS levels in lung cancer cells after intermittent intervention with DDP. Methods: The sensitivity of A549 cells to DDP was detected by cck-8 method, A549 cells were treated by DDP intermitten, 6PGD protein expression was detected by Western blot method, and the ROS level of A549 cells was determined by ROS kit. NADPH levels of A549 cells were determined by NADPH kit. Result: After DDP intermittent intervention, the expression of 6PGD protein in lung cancer cells A549 was increased, the growth and migration of A549 cells were significantly inhibited, and ROS and NADPH levels were significantly increased. Conclusion: 6PGD were upregulated in after DDP intermittent intervention and affected the migration ability in lung cancer cells.

Effect of anamorelin/ONO-7643, a selective ghrelin receptor agonist, on tumor growth in a lung cancer mouse xenograft model.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. e19577-e19577
Author(s):  
Robert Northrup ◽  
Ken Kuroda ◽  
Elizabeth Manning Duus ◽  
Sheri Routt Barnes ◽  
Tim Wiley ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Body Weight ◽  
Tumor Growth ◽  
Food Consumption ◽  
Nude Mice ◽  
Receptor Agonist ◽  
Xenograft Model ◽  
Ghrelin Receptor ◽  
Mouse Xenograft Model ◽  
Ghrelin Receptor Agonist

e19577 Background: Anamorelin/ONO-7643 is an orally-active ghrelin receptor agonist in development for non-small cell lung cancer (NSCLC)-related cachexia/anorexia. It displays both anabolic and orexigenic properties via its ghrelin and growth hormone (GH) secretagogue activity. However, increasing GH and insulin-like growth factor-1 (IGF-1) in cancer patients raises potential concerns of stimulating tumor growth. In this study, we investigated the effect of ghrelin and Anamorelin/ONO-7643 on tumor growth in a NSCLC xenograft model. Methods: On Day 1 (D1), 21 days after implanting A549 tumors, female nude mice were sorted into six groups (n=15/group) and administered ghrelin (2 mg/kg i.p.), Anamorelin/ONO-7643 (3, 10, or 30 mg/kg p.o.) or vehicles (saline i.p. or de-ionized water p.o.) for 28 days, starting on D3. Tumor growth, body weight, and food consumption were monitored. Mice used to assess plasma levels of murine GH (mGH) and IGF-1 (mIGF-1) were sorted into three groups (n=21/group) and treated for 28 days with ghrelin, the high dose of Anamorelin/ONO-7643 or vehicle (de-ionized water p.o.). Results: After 28 days of treatment, there was no difference in median tumor volumes (D30 values: 1008, 936, 1080, 666 and 847 mm3 for vehicle, ghrelin and Anamorelin/ONO-7643 at 3, 10 and 30 mg/kg, respectively). Ghrelin significantly increased mGH compared to controls, while Anamorelin/ONO-7643 modestly increased mGH. Peak mIGF-1 levels were slightly higher in animals given ghrelin or Anamorelin/ONO-7643 compared to vehicle, although not significantly. Anamorelin/ONO-7643 at 10 and 30 mg/kg/day showed a statistically significant (p<0.01) increase in body weight from D1 to D30 compared to control animals, with no change in food consumption. Ghrelin treatment had no effect on body weight or food consumption. Conclusions: Anamorelin/ONO-7643 or ghrelin treatment for 28 days had no effect on tumor growth in A549 tumor-bearing nude mice, despite increased mGH and a trend of increased mIGF-1. Anamorelin/ONO-7643 also significantly increased body weight at 10 and 30 mg/kg/day. These results support using ghrelin receptor agonist-based treatments in managing NSCLC-related cachexia/anorexia.

scholarly journals Development and Characterization of Patient-Derived Xenografts from Non-Small Cell Lung Cancer Brain Metastases

2020 ◽  
Author(s):  
Andrew M. Baschnagel ◽  
Saakshi Kaushik ◽  
Arda Durmaz ◽  
Steve Goldstein ◽  
Irene M. Ong ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Brain Metastases ◽  
Tumor Growth ◽  
Small Cell Lung Cancer ◽  
Cell Lines ◽  
Cell Lung Cancer ◽  
Xenograft Model ◽  
Small Cell ◽  
Growth Delay ◽  
Small Cell Lung

AbstractIntroductionThe purpose of this study was to establish and characterize a direct-from patient-derived xenograft (PDX) model of non-small cell lung cancer (NSCLC) brain metastases.MethodsSurgically obtained tissue was implanted subcutaneously and as orthotopic intracranial implants into immunodeficient mice. Histology and DNA loci were compared between original tumor and subsequent PDX passages. Tumors underwent RNA and DNA sequencing and relevant therapeutic targets were identified. Tumor growth rates were assessed following treatment with radiation, MEK inhibitor selumetinib, or MET inhibitor savolitinib. Cell lines were established.ResultsNine NSCLC brain metastases PDXs were established. Morphologically, strong retention of cytoarchitectural features was observed between original patient tumor and subcutaneous and intracranial tumors. Short tandem repeat analysis demonstrated strong concordance between patient tumors and subsequent PDX passages. Transcriptome and mutation analysis revealed high correlation between matched patient and PDX samples. Significant growth inhibition occurred with radiation, with selumetinib in tumors harboring KRAS G12C mutations and with savolitinib in a tumor with MET exon 14 skipping mutation. The combination of radiation and savolitinib resulted in significant tumor growth delay compared to radiation or savolitinib alone our MET exon 14 skipping mutation PDX. Early passage cell strains showed high consistency between patient and PDX tumors.ConclusionWe have established a robust human xenograft model system for investigating NSCLC brain metastases. These PDXs and cell lines show strong phenotypic and molecular correlation with the original patient tumors and provide a valuable resource for testing preclinical therapeutics.

scholarly journals In vivo Tumor Growth and Spontaneous Metastasis Assays Using A549 Lung Cancer Cells

BIO-PROTOCOL ◽  
2020 ◽  
Vol 10 (7) ◽  
Author(s):  
Lei Qi ◽  
Teresa Knifley ◽  
Dava Piecoro ◽  
Piotr Rychahou ◽  
Jianrong Wu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Spontaneous Metastasis ◽  
A549 Lung
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