scholarly journals Intravital Fluorescence Facilitates Measurement of Multiple Physiologic Functions and Gene Expression in Tumors of Live Animals

2002 ◽  
Vol 18 (5-6) ◽  
pp. 293-311 ◽  
Author(s):  
Mark W. Dewhirst ◽  
S. Shan ◽  
Yiting Cao ◽  
Benjamin Moeller ◽  
Fan Yuan ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Fluorescence Imaging ◽  
Flow Instability ◽  
Modern Medicine ◽  
Normal Tissues ◽  
Fluorescent Markers ◽  
Functional Differences ◽  
Real Time Visualization ◽  
Window Chamber

The purpose of this report is to present an overview of the use of fluorescence imagingin vivo, with particular emphasis on oncology. It is important to note, however, that many of the methods described herein have been applied to the study of non-malignant tissues as well. Modern medicine and biology research has benefited greatly from an ever-expanding assortment of fluorescent markers and labels. These markers and labels have allowed investigators to observe the behavior and properties of cell and molecular entities of interest in the context of complicated biological systems such as a mammalian cell or a whole mouse. Methods developed to image fluorescence in whole mice have been valuable in studying patterns of tumor growth and metastases. Alternatively, more detailed information and a wide variety of endpoints can be obtained using “intravital” preparations. This review focuses on use of fluorescence imaging for intravital preparations. For detail on fluorescence imaging of whole animals, refer to reviews on this subject [1,2]. For oncologic applications, studies have focused primarily on window chamber preparations that allow for real-time visualization of tumor growth, vascularity, vascular responses to stimulation, vascular permeability, vascular orientation, flow instability, and the like. These endpoints have been used to show that there are functional differences between tumor and normal tissues with respect to these functions under baseline conditions and after therapeutic manipulation. Examples of some of these differences are provided in this review as a means to illustrate how they can be used.

scholarly journals Monitoring of Xenograft Tumor Growth and Response to Chemotherapy by Non-Invasive In Vivo Multispectral Fluorescence Imaging

PLoS ONE ◽  
2012 ◽  
Vol 7 (10) ◽  
pp. e47927 ◽  
Author(s):  
Henrike Caysa ◽  
Stefan Hoffmann ◽  
Jana Luetzkendorf ◽  
Lutz Peter Mueller ◽  
Susanne Unverzagt ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Fluorescence Imaging ◽  
Xenograft Tumor ◽  
Non Invasive ◽  
Response To Chemotherapy ◽  
Xenograft Tumor Growth ◽  
Multispectral Fluorescence Imaging

In vivo real-time visualization of mesenchymal stem cells tropism for cutaneous regeneration using NIR-II fluorescence imaging

Biomaterials ◽  
2015 ◽  
Vol 53 ◽  
pp. 265-273 ◽  
Author(s):  
Guangcun Chen ◽  
Fei Tian ◽  
Chunyan Li ◽  
Yejun Zhang ◽  
Zhen Weng ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Real Time ◽  
Fluorescence Imaging ◽  
Real Time Visualization

scholarly journals Degradation of long non-coding RNA-CIR decelerates proliferation, invasion and migration, but promotes apoptosis of osteosarcoma cells

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Shiwei Liu ◽  
Jingchao Li ◽  
Liang Kang ◽  
Yueyang Tian ◽  
Yuan Xue
Keyword(s):  
Tumor Growth ◽  
Osteosarcoma Cell ◽  
Loss Of Function ◽  
Osteosarcoma Cells ◽  
Invasion And Migration ◽  
Normal Tissues ◽  
Novel Target ◽  
And Migration

Abstract Background Over the years, long non-coding RNAs (lncRNAs) have been clarified in malignancies, this research was focused on the role of lncRNA cartilage injury-related (lncRNA-CIR) in osteosarcoma cells. Methods LncRNA-CIR expression in osteosarcoma tissues and cells, and adjacent normal tissues and normal osteoblasts was determined, then the relations between lncRNA-CIR expression and the clinicopathological features, and between lncRNA-CIR expression and the prognosis of osteosarcoma patients were analyzed. Moreover, the MG63 and 143B cells were treated with silenced or overexpressed lncRNA-CIR, and then the proliferation, invasion, migration and apoptosis of the cells were evaluated by gain- and loss-of-function approaches. The tumor growth, and proliferation and apoptosis of osteosarcoma cells in vivo were observed by subcutaneous tumorigenesis in nude mice. Results We have found that lncRNA-CIR was up-regulated in osteosarcoma tissues and cells, which was respectively relative to adjacent normal tissues and normal osteoblasts. The expression of lncRNA-CIR was evidently correlated with disease stages, distant metastasis and differentiation of osteosarcoma patients, and the high expression of lncRNA-CIR indicated a poor prognosis. Furthermore, the reduction of lncRNA-CIR could restrict proliferation, invasion and migration, but promote apoptosis of osteosarcoma cells in vitro. Meanwhile, inhibited lncRNA-CIR also restrained tumor growth and osteosarcoma cell proliferation, whereas accelerated apoptosis of osteosarcoma cells in vivo. Conclusion We have found in this study that the inhibited lncRNA-CIR could decelerate proliferation, invasion and migration, but accelerate apoptosis of osteosarcoma cells, which may provide a novel target for osteosarcoma treatment.

A method to follow tumor growth and tumor induced bone loss simultaneously over time, in vivo, using whole body bioluminescence fluorescence imaging

Bone ◽  
2011 ◽  
Vol 48 (1) ◽  
pp. S49-S50
Author(s):  
T.J.A. Snoeks* ◽  
A. Khmelinskii ◽  
I. Que ◽  
B. Lelieveldt ◽  
E.L. Kaijzel ◽  
...  
Keyword(s):  
Bone Loss ◽  
Tumor Growth ◽  
Fluorescence Imaging ◽  
Whole Body ◽  
Over Time

scholarly journals Biocompatible Mesoporous Silica–Polydopamine Nanocomplexes as MR/Fluorescence Imaging Agent for Light-Activated Photothermal–Photodynamic Cancer Therapy In Vivo

2021 ◽  
Vol 9 ◽  
Author(s):  
Jiahui Lu ◽  
Chen Ni ◽  
Jie Huang ◽  
Yawen Liu ◽  
Yingkai Tao ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Mesoporous Silica ◽  
Fluorescence Imaging ◽  
Colloidal Stability ◽  
Silica Nanoparticle ◽  
Photothermal Conversion ◽  
Normal Tissues ◽  
Irradiation Power

Conventional cancer phototherapy with single modality suffers from low therapeutic efficacy and undesired posttreatment damage for adjacent normal tissues. Therefore, the lower NIR laser irradiation power is vital to the reduction or preclusion of risk of scalds and burns in normal tissues. Herein, we rationally proposed a novel multifunctional nanocomplex, which enabled good magnetic resonance (MR) imaging contrast effect and promising photothermal conversion efficacy. The prepared core/shell nanocomplexes [MSN-Ce6@PDA (Mn)] were composed of chlorin e6-embedded mesoporous silica/nanoparticle composites as the cores, and then polydopamine and manganese ions were conjugated on the cores to form protective shells. The MSN-Ce6@PDA (Mn) nanocomplexes revealed superior properties in colloidal stability, photothermal conversion, reaction oxygen species generation, magnetic resonance imaging, etc. Under the guidance of MR and fluorescence imaging, these MSN-Ce6@PDA (Mn) nanocomplexes were found to be primarily accumulated in the MDA-MB-231 tumor area. Furthermore, the combined photodynamic and photothermal therapy exhibited strong inhibition to the growth of MDA-MB-231 tumor in vitro and in vivo. Besides, the MSN-Ce6@PDA (Mn) nanocomplexes also exhibited excellent biocompatibility and low damage to the healthy animals. Hence, the results demonstrated that the prepared MSN-Ce6@PDA (Mn) nanocomplex would be a promising potential for multimodal imaging-guided phototherapy.

scholarly journals Fibroblast Growth Factor 11 (FGF11) Promotes Non-small Cell Lung Cancer (NSCLC) Progression by Regulating Hypoxia Signaling Pathway

2021 ◽  
Author(s):  
Xiaowei Wu ◽  
Minjie Li ◽  
Yu Deng ◽  
Shun Ke ◽  
Fan Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Growth ◽  
Signaling Pathway ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Normal Tissues ◽  
Tumor Tissues ◽  
Hypoxia Signaling

Abstract Background: Recently, accumulating studies highlight the critical regulatory roles of fibroblast growth factors (FGF), and a series of FGF, participated in the progression of multiple human cancers, including non-small cell lung cancer (NSCLC). Methods: Gene transcriptome analysis was used to identify the differential expression of FGF11 in NSCLC tumor tissues, GSE75037 and GSE81089 database analysis was performed on NSCLC tumor tissues and adjacent normal tissues to validate the expression of FGF11. Then, we selected 100 cases of NSCLC tumor tissues and 30 cases of matched adjacent normal tissues to confirm the mRNA and protein level of FGF11 by qRT-PCR and immunohistochemistry. Bioinformatics analysis and dual luciferase reporter analysis was also performed to examine the direct regulatory of FGF11 by miR-525-5p. CCK-8 and transwell assay was also performed to detect the cell proliferation, migration and invasion. Signal pathway analysis was also investigated the effect of FGF11 on NSCLC cell proliferation was associated with the hypoxia signaling pathway. The role of FGF11 in NSCLC tumor growth was further explored by in vivo study.Results: FGF11 was overexpressed in NSCLC tumor tissues and tumor cell lines, the high expression of FGF11 was closely associated with poor overall survival of NSCLC patients. In vitro loss- and gain- of function experiments demonstrated that FGF11 knockdown inhibited, whereas FGF11 overexpression promoted the proliferation, migration and invasion of NSCLC cells. The dual luciferase reporter assay confirmed that FGF11 was downregulated by miR-525-5p, and the effect of FGF11 on cell proliferation, migration and invasion could be interfered by miR-525-5p. We further found that FGF11 had significant correlation with hypoxia signaling pathway activation, meanwhile regulating HIF-1α. Further experiments implicated that the oncogenic role of FGF11 could be blocked via interfering of HIF-1α in NSCLC cells. Moreover, knockdown of FGF11 suppressed NSCLC tumor growth whereas overexpression of FGF11 promoted tumor growth in vivo. Conclusions: FGF11 might be functioned as an oncogene in tumor development, the findings of our study revealed a novel regulatory mechanism of FGF11 involved in hypoxia signaling pathway, which offers novel strategies for the treatment of NSCLC.

In vivo multi-modality photoacoustic and pulse echo tracking of prostate tumor growth using a window chamber

2010 ◽  
Author(s):  
Daniel R. Bauer ◽  
Ragnar Olafsson ◽  
Leonardo G. Montilla ◽  
Russell S. Witte
Keyword(s):  
Tumor Growth ◽  
Prostate Tumor ◽  
Echo Tracking ◽  
Pulse Echo ◽  
Window Chamber

scholarly journals PBX3 Promotes Tumor Growth and Angiogenesis via Activation of AT1R/VEGFR2 Pathway in Papillary Thyroid Carcinoma

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Qin Chen ◽  
Wen-Ying Yu ◽  
Huan-Huan Zhang ◽  
Song-Zhao Zhang ◽  
Jie Fang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Tumor Growth ◽  
Papillary Thyroid ◽  
Normal Tissues ◽  
Cycle Arrest ◽  
B Cell Leukemia

PBX3 (Pre-B-cell leukemia homeobox 3) had been considered to be a multifunctional oncogene which involved in tumor growth, invasion, and metastasis in leukemia and some solid tumors. However, the contribution of PBX3 to papillary thyroid carcinoma (PTC) remains unclear. In this study, we found that PBX3 expression was significantly upregulated in PTC tissues compared to adjacent normal tissues, and high levels of PBX3 were correlated with tumor size, lymphatic metastasis, TMN stage, and poor prognosis of PTC patients. Overexpression of PBX3 in PTC cell lines promoted cell proliferation. Consistently, knockdown of PBX3 by shRNA induced cell cycle arrest at G0/G1 phase, and inhibited angiogenesis and tumor growth in vitro and in vivo. Furthermore, PBX3 promoted PTC cell proliferation and angiogenesis through activation of AT1R/VEGFR2 pathway while overexpression of AT1R and treatment with VEGFA reversed PBX3-shRNA-induced decreased phosphorylation of VEGFR2 and its downstream (ERK1/2, AKT and Src). It demonstrated that PBX3 could be used as a potential prognostic biomarker and therapeutic target for PTC.

scholarly journals In Vivo Fluorescence Imaging and Urinary Monoamines as Surrogate Biomarkers of Disease Progression in a Mouse Model of Pheochromocytoma

Endocrinology ◽  
2014 ◽  
Vol 155 (11) ◽  
pp. 4149-4156 ◽  
Author(s):  
Martin Ullrich ◽  
Ralf Bergmann ◽  
Mirko Peitzsch ◽  
Marc Cartellieri ◽  
Nan Qin ◽  
...  
Keyword(s):  
Mouse Model ◽  
Tumor Growth ◽  
Tumor Progression ◽  
Fluorescence Imaging ◽  
Fluorescence Intensity ◽  
Tumor Development ◽  
Treatment Strategies ◽  
Small Animal ◽  
Whole Body

Abstract Pheochromocytoma (PHEO) is a rare but potentially lethal neuroendocrine tumor arising from catecholamine-producing chromaffin cells. Especially for metastatic PHEO, the availability of animal models is essential for developing novel therapies. For evaluating therapeutic outcome in rodent PHEO models, reliable quantification of multiple organ lesions depends on dedicated small-animal in vivo imaging, which is still challenging and only available at specialized research facilities. Here, we investigated whether whole-body fluorescence imaging and monitoring of urinary free monoamines provide suitable parameters for measuring tumor progression in a murine allograft model of PHEO. We generated an mCherry-expressing mouse PHEO cell line by lentiviral gene transfer. These cells were injected subcutaneously into nude mice to perform whole-body fluorescence imaging of tumor development. Urinary free monoamines were measured by liquid chromatography with tandem mass spectrometry. Tumor fluorescence intensity and urinary outputs of monoamines showed tumor growth–dependent increases (P < .001) over the 30 days of monitoring post-tumor engraftment. Concomitantly, systolic blood pressure was increased significantly during tumor growth. Tumor volume correlated significantly (P < .001) and strongly with tumor fluorescence intensity (rs = 0.946), and urinary outputs of dopamine (rs = 0.952), methoxytyramine (rs = 0.947), norepinephrine (rs = 0.756), and normetanephrine (rs = 0.949). Dopamine and methoxytyramine outputs allowed for detection of lesions at diameters below 2.3 mm. Our results demonstrate that mouse pheochromocytoma (MPC)-mCherry cell tumors are functionally similar to human PHEO. Both tumor fluorescence intensity and urinary outputs of free monoamines provide precise parameters of tumor progression in this sc mouse model of PHEO. This animal model will allow for testing new treatment strategies for chromaffin cell tumors.

scholarly journals Exosomal circEIF3K from cancer-associated fibroblast promotes colorectal cancer (CRC) progression via miR-214/PD-L1 axis

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Kaihua Yang ◽  
Jie Zhang ◽  
Chuanqing Bao
Keyword(s):  
Tumor Microenvironment ◽  
Tumor Growth ◽  
Tube Formation ◽  
Normal Tissues ◽  
Cancer Associated Fibroblast ◽  
Dataset Analysis ◽  
Tcga Dataset ◽  
Sw620 Cells ◽  
Hct116 Cells

Abstract Background Tumor microenvironment (e.g., cancer-associated fibroblast) plays a key role in cancer tumorigenesis and metastasis. However, the detailed mechanism of whether hypoxia promotes CRC progression via tumor microenvironment remains unclear. Methods In this study, circEIF3K exosome was examined by NanoSight Tracking Analysis and RT-qPCR. We used cell colony formation assay, transwell assay and tube formation assay to determine proliferation, invasion and metastasis of HCT116 or SW620 cells. Xenograft tumor assay was employed to show in vivo tumor growth of HCT116 cells. Results We found that hypoxia could induce secretion of circEIF3K exosome. Conditioned medium (CM) and exosome from circEIF3K knockdown CAF significantly attenuated proliferation, invasion and tube formation of HCT116 or SW620 cells, which could be reverted by miR-214 under hypoxia treatment. Besides, we observed that circEIF3K knockdown evidently impaired tumor growth in mice. TCGA dataset analysis showed that low expression of circEIF3K was observed in normal tissues and associated with prolonged survival time. Finally, PD-L1 was confirmed as important target for miR-214 in CRC. Conclusion In conclusion, our study reveals that a novel axis circEIF3K/miR-214/PD-L1 mediates hypoxia-induced CRC progression via CAF, providing the rationale for developing new targeted therapeutics to treat CRC.

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