scholarly journals Longitudinal assessment of lung cancer progression in the mouse using in vivo micro-CT imaging

2010 ◽  
Vol 37 (9) ◽  
pp. 4793-4805 ◽  
Author(s):  
Eman Namati ◽  
Jacqueline Thiesse ◽  
Jessica C. Sieren ◽  
Alan Ross ◽  
Eric A. Hoffman ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Progression ◽  
Ct Imaging ◽  
Micro Ct ◽  
Longitudinal Assessment

scholarly journals Longitudinal Assessment of Lung Cancer Progression in Mice Using the Sodium Iodide Symporter Reporter Gene and SPECT/CT Imaging

PLoS ONE ◽  
2016 ◽  
Vol 11 (12) ◽  
pp. e0169107 ◽  
Author(s):  
Dominique N. Price ◽  
Amber A. McBride ◽  
Martina Anton ◽  
Donna F. Kusewitt ◽  
Jeffrey P. Norenberg ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Reporter Gene ◽  
Cancer Progression ◽  
Sodium Iodide ◽  
Ct Imaging ◽  
Sodium Iodide Symporter ◽  
Longitudinal Assessment

scholarly journals Circular RNA FLNA acts as a sponge of miR-486-3p in promoting lung cancer progression via regulating XRCC1 and CYP1A1

2021 ◽  
Author(s):  
Jiongwei Pan ◽  
Gang Huang ◽  
Zhangyong Yin ◽  
Xiaoping Cai ◽  
Enhui Gong ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cancer Progression ◽  
Lung Cancer Cells ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Related Factors

AbstractSignificantly high-expressed circFLNA has been found in various cancer cell lines, but not in lung cancer. Therefore, this study aimed to explore the role of circFLNA in the progression of lung cancer. The target gene of circFLNA was determined by bioinformatics and luciferase reporter assay. Viability, proliferation, migration, and invasion of the transfected cells were detected by CCK-8, colony formation, wound-healing, and transwell assays, respectively. A mouse subcutaneous xenotransplanted tumor model was established, and the expressions of circFLNA, miR-486-3p, XRCC1, CYP1A1, and related genes in the cancer cells and tissues were detected by RT-qPCR, Western blot, or immunohistochemistry. The current study found that miR-486-3p was low-expressed in lung cancer. MiR-486-3p, which has been found to target XRCC1 and CYP1A1, was regulated by circFLNA. CircFLNA was located in the cytoplasm and had a high expression in lung cancer cells. Cancer cell viability, proliferation, migration, and invasion were promoted by overexpressed circFLNA, XRCC1, and CYP1A1 but inhibited by miR-486-3p mimic and circFLNA knockdown. The weight of the xenotransplanted tumor was increased by circFLNA overexpression yet reduced by miR-486-3p mimic. Furthermore, miR-486-3p mimic reversed the effect of circFLNA overexpression on promoting lung cancer cells and tumors and regulating the expressions of miR-486-3p, XRCC1, CYP1A1, and metastasis/apoptosis/proliferation-related factors. However, overexpressed XRCC1 and CYP1A1 reversed the inhibitory effect of miR-486-3p mimic on cancer cells and tumors. In conclusion, circFLNA acted as a sponge of miR-486-3p to promote the proliferation, migration, and invasion of lung cancer cells in vitro and in vivo by regulating XRCC1 and CYP1A1.

scholarly journals POU2F2 promotes the proliferation and motility of lung cancer cells by activating AGO1

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ronggang Luo ◽  
Yi Zhuo ◽  
Quan Du ◽  
Rendong Xiao
Keyword(s):  
Lung Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Cancer Tissues

Abstract Background To detect and investigate the expression of POU domain class 2 transcription factor 2 (POU2F2) in human lung cancer tissues, its role in lung cancer progression, and the potential mechanisms. Methods Immunohistochemical (IHC) assays were conducted to assess the expression of POU2F2 in human lung cancer tissues. Immunoblot assays were performed to assess the expression levels of POU2F2 in human lung cancer tissues and cell lines. CCK-8, colony formation, and transwell-migration/invasion assays were conducted to detect the effects of POU2F2 and AGO1 on the proliferaion and motility of A549 and H1299 cells in vitro. CHIP and luciferase assays were performed for the mechanism study. A tumor xenotransplantation model was used to detect the effects of POU2F2 on tumor growth in vivo. Results We found POU2F2 was highly expressed in human lung cancer tissues and cell lines, and associated with the lung cancer patients’ prognosis and clinical features. POU2F2 promoted the proliferation, and motility of lung cancer cells via targeting AGO1 in vitro. Additionally, POU2F2 promoted tumor growth of lung cancer cells via AGO1 in vivo. Conclusion We found POU2F2 was highly expressed in lung cancer cells and confirmed the involvement of POU2F2 in lung cancer progression, and thought POU2F2 could act as a potential therapeutic target for lung cancer.

scholarly journals Volumetric Imaging of Lung Tissue at Micrometer Resolution: Clinical Applications of Micro-CT for the Diagnosis of Pulmonary Diseases

Diagnostics ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 2075
Author(s):  
Andreana Bompoti ◽  
Andreas S. Papazoglou ◽  
Dimitrios V. Moysidis ◽  
Nikolaos Otountzidis ◽  
Efstratios Karagiannidis ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Tissue ◽  
Lung Diseases ◽  
Human Lung ◽  
Imaging Modality ◽  
Clinical Applications ◽  
Ct Imaging ◽  
Micro Ct ◽  
Volumetric Imaging ◽  
Scoping Reviews

Micro-computed tomography (micro-CT) is a promising novel medical imaging modality that allows for non-destructive volumetric imaging of surgical tissue specimens at high spatial resolution. The aim of this study is to provide a comprehensive assessment of the clinical applications of micro-CT for the tissue-based diagnosis of lung diseases. This scoping review was conducted in accordance with the PRISMA Extension for Scoping Reviews, aiming to include every clinical study reporting on micro-CT imaging of human lung tissues. A literature search yielded 570 candidate articles, out of which 37 were finally included in the review. Of the selected studies, 9 studies explored via micro-CT imaging the morphology and anatomy of normal human lung tissue; 21 studies investigated microanatomic pulmonary alterations due to obstructive or restrictive lung diseases, such as chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, and cystic fibrosis; and 7 studies examined the utility of micro-CT imaging in assessing lung cancer lesions (n = 4) or in transplantation-related pulmonary alterations (n = 3). The selected studies reported that micro-CT could successfully detect several lung diseases providing three-dimensional images of greater detail and resolution than routine optical slide microscopy, and could additionally provide valuable volumetric insight in both restrictive and obstructive lung diseases. In conclusion, micro-CT-based volumetric measurements and qualitative evaluations of pulmonary tissue structures can be utilized for the clinical management of a variety of lung diseases. With micro-CT devices becoming more accessible, the technology has the potential to establish itself as a core diagnostic imaging modality in pathology and to enable integrated histopathologic and radiologic assessment of lung cancer and other lung diseases.

scholarly journals Metabolic breakdown of non-small cell lung cancers by mitochondrial HSPD1 targeting

2021 ◽  
Author(s):  
Beatrice Parma ◽  
Vignesh Ramesh ◽  
Paradesi Naidu Gollavilli ◽  
Aarif Siddiqui ◽  
Luisa Pinna ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Progression ◽  
Therapeutic Potential ◽  
Small Cell ◽  
Small Cell Lung ◽  
Lung Cancers ◽  
Metabolism Enzymes ◽  
Shock Proteins

ABSTRACTThe identification of novel targets is of paramount importance to develop more effective drugs and improve the treatment of non-small cell lung cancer (NSCLC), the leading cause of cancer-related deaths worldwide. Since cells alter their metabolic rewiring during tumorigenesis and along cancer progression, targeting key metabolic players and metabolism-associated proteins represents a valuable approach with a high therapeutic potential. Metabolic fitness relies on the functionality of heat shock proteins (HSPs), molecular chaperones that facilitate the correct folding of metabolism enzymes and their assembly in macromolecular structures. Here, we show HSPD1 (HSP60) as a survival gene ubiquitously expressed in NSCLC and associated with poor patients’ prognosis. HSPD1 knockdown or its chemical disruption by the small molecule KHS101 induces a drastic breakdown of oxidative phosphorylation, and suppresses cell proliferation both in vitro and in vivo. By combining drug profiling with transcriptomics and through a whole-genome CRISPR/Cas9 screen, we demonstrate that HSPD1-targeted anti-cancer effects are dependent on OXPHOS and validated molecular determinants of KHS101 sensitivity, in particular, the creatine-transporter SLC6A8 and the subunit of the cytochrome c oxidase complex COX5B. These results highlight mitochondrial metabolism as an attractive target and HSPD1 as a potential theranostic marker for developing therapies to combat NCSLC.SignificanceHSPD1 elimination or disruption interferes with NSCLC metabolic activity causing a strong OXPHOS-dependent energetic breakdown, which the cancer cells fail to overcome, highlighting HSPD1 as a potential theranostic marker for improving lung cancer therapy.

scholarly journals The Role of Cavin3 in the Progression of Lung Cancer and Its Mechanism

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Gaozhong Sun ◽  
Kewei Ni
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Tumor Formation ◽  
Migration And Invasion ◽  
Clinical Value ◽  
Promote Cell Proliferation ◽  
Cancer Tissues

Objective. The purpose of this study was to describe the role of Cavin3 in the progression of lung cancer and its underlying mechanism. Methods. Totally, 200 cases of lung cancer tissues and corresponding paracancer tissues were collected. Cavin3 expression in samples was determined by qRT-PCR, and the correlation with lung cancer stages as well as prognosis was statistically analyzed combined with matched clinical information. To investigate the mechanism of Cavin3 in lung cancer progression, firstly, Cavin3 was detected in lung cancer cell lines A549, PC9, and H520. Then, cells with stable Cavin3 overexpression and Cavin3 knockout were established to determine the effect of Cavin3 overexpression on the mammalian target of rapamycin (mTOR) signaling pathway. Subsequently, cells were harvested for cell proliferation, migration, and invasion assays in vitro, as well as nude mouse transplantation tumor experiment in vivo. Results. Cavin3 was seen to be highly expressed in cancer tissues. Statistical analysis with matched clinical data showed that Cavin3 as a prognostic indicator of lung cancer had important clinical value. In addition, it could be found that high expression of Cavin3 was able to promote cell proliferation, migration, and invasion and also potentiate tumor formation in vivo. Conclusion. Cavin3 was highly expressed in lung cancer, and it was capable to promote cell proliferation, invasion, and migration.

scholarly journals Effects of long-term in vivo micro-CT imaging on hallmarks of osteopenia and frailty in aging mice

PLoS ONE ◽  
2020 ◽  
Vol 15 (9) ◽  
pp. e0239534
Author(s):  
Ariane C. Scheuren ◽  
Gisela A. Kuhn ◽  
Ralph Müller
Keyword(s):  
Ct Imaging ◽  
Micro Ct

Radiosensitization and micro CT imaging of multifunctional gold nanoparticles in lung adenocarcinoma A549 cell: An in vivo animal study.

2018 ◽  
Vol 36 (15_suppl) ◽  
pp. e20557-e20557
Author(s):  
Tao Li ◽  
Chuan Yang ◽  
Guojun Zhang ◽  
Jianming Huang ◽  
Jiahua Lv ◽  
...  
Keyword(s):  
Gold Nanoparticles ◽  
Lung Adenocarcinoma ◽  
Animal Study ◽  
A549 Cell ◽  
Ct Imaging ◽  
Micro Ct ◽  
Lung Adenocarcinoma A549

scholarly journals Anti- and Protumorigenic Effects of PPARγin Lung Cancer Progression: A Double-Edged Sword

PPAR Research ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Howard Li ◽  
Mary C. M. Weiser-Evans ◽  
Raphael Nemenoff
Keyword(s):  
Lung Cancer ◽  
Cancer Progression ◽  
Peroxisome Proliferator ◽  
Lung Carcinogenesis ◽  
Cancer Treatments ◽  
Peroxisome Proliferator Activated Receptor ◽  
Control Of Gene Expression ◽  
Inhibition Of Growth

Peroxisome proliferator-activated receptor-γ(PPARγ) is a member of the nuclear receptor superfamily of ligand-activated transcription factors that plays an important role in the control of gene expression linked to a variety of physiological processes, including cancer. Ligands for PPARγinclude naturally occurring fatty acids and the thiazolidinedione class of antidiabetic drugs. Activation of PPARγin a variety of cancer cells leads to inhibition of growth, decreased invasiveness, reduced production of proinflammatory cytokines, and promotion of a more differentiated phenotype. However, systemic activation of PPARγhas been reported to be protumorigenic in somein vitrosystems andin vivomodels. Here, we review the available data that implicate PPARγin lung carcinogenesis and highlight the challenges of targeting PPARγin lung cancer treatments.

Sign in / Sign up

Export Citation Format

Share Document