scholarly journals Cetuximab-Conjugated Perfluorohexane/Gold Nanoparticles for Low Intensity Focused Ultrasound Diagnosis Ablation of Thyroid Cancer Treatment

2020 ◽  
Author(s):  
Yue Ma ◽  
Lingling Wang ◽  
Haixia Li ◽  
Wen Cheng ◽  
Xiulan Zheng ◽  
...  

Abstract Chemotherapeutic efficacy can be significantly developed nanotheranostics systems of drug delivery in tumor cells. In this work, we have demonstrated that the self-assembled by C225 conjugates Au-PFH-NPs (C-Au-PFH-NPs) for low intensity focused ultrasound diagnosis ablation of thyroid cancer treatment. C-Au-PFH-NPs have shown excellent stability in water, PBS and 20% rat serum. Transmission electron microscopy (TEM) images also exposed the effective construction of C-Au-PFH-NPs with commonly spherical sized assemblies. The incubation of the C625 thyroid carcinoma with C-Au-PFH-NPs triggers apoptosis, which was confirmed by the flowcytometry analysis. The C-Au-PFH-NPs, with remarkably displays the potent antitumor efficacy in a human thyroid carcinoma xenografts. A histopathological result reveals that precisely achieved to additional confirm these outcomes. Further, we successfully examined the efficiency of C-Au-PFH-NPs when used the thyroid carcinoma low intensity focused ultrasound diagnosis imaging (LIFUS) in vivo. These findings clearable for LIFUS agents with high performing image and different therapeutic purpose will have extensive possible for the future biomedical purposes.

Author(s):  
Yue Ma ◽  
Lingling Wang ◽  
Haixia Li ◽  
Wen Cheng ◽  
Xiulan Zheng ◽  
...  

Abstract Chemotherapeutic efficacy plays a significant role in the development of nanotheranostic systems for drug delivery in tumor cells. In this study, we demonstrate the self-assembly of C225 conjugate, Perfluorohexane/Gold Nanoparticles (Au-PFH-NPs), which results in low-intensity focused ultrasound diagnosis ablation of thyroid cancer treatment. Cetuximab-Conjugated Perfluorohexane/Gold Nanoparticles (C-Au-PFH-NPs) showed excellent stability in water, PBS, and 20% rat serum. Transmission electron microscopy images revealed the effective construction of C-Au-PFH-NPs with commonly spherical assemblies. The incubation of C625 thyroid carcinoma with C-Au-PFH-NPs triggered apoptosis, which was confirmed by flow cytometry analysis. The C-Au-PFH-NPs showed remarkable antitumor efficacy in human thyroid carcinoma xenografts. The histopathological results additionally confirm the achieved outcomes. Furthermore, we successfully examined the efficiency of C-Au-PFH-NPs when using the thyroid carcinoma low-intensity focused ultrasound (LIFUS) diagnostic imaging in vivo. These findings are clear for LIFUS agents with high performing images. It is also identified that different therapeutic purposes will have extensive potential for future biomedical purposes.


2020 ◽  
Author(s):  
Ming Qi ◽  
Yufeng Zhu ◽  
Wenjuan Wang ◽  
Shufeng Gao ◽  
Sihui Nie ◽  
...  

Abstract Chemotherapeutic efficacy can be significantly developed nanotheranostics systems of drug delivery in tumor cells. In this work, we have demonstrated that the self-assembled by C225 conjugates Gd-PFH-NPs (C-Gd-PFH-NPs) for low intensity focused ultrasound diagnosis ablation of thyroid cancer treatment. C-Gd-PFH-NPs have shown excellent stability in PBS. Transmission electron microscopy (TEM) images also exposed the effective construction of C-Gd-PFH-NPs with commonly spherical sized assemblies. The incubation of the C625 thyroid carcinoma with C-Gd-PFH-NPs triggers apoptosis, which was confirmed by the flowcytometry analysis. The C-Gd-PFH-NPs, with remarkably displays the potent antitumor efficacy in a human C625 thyroid carcinoma xenografts. A histopathological result reveals that precisely achieved to additional confirm these outcomes. Further, we successfully examined the efficiency of C-Gd-PFH-NPs when used the thyroid carcinoma low intensity focused ultrasound diagnosis imaging (LIFUS) in vivo. These findings clearable for LIFUS agents with high performing image and different therapeutic purpose will have extensive possible for the future biomedical purposes.


2021 ◽  
Vol 14 (1) ◽  
pp. 38
Author(s):  
Hyo Jeong Lee ◽  
Pyeonghwa Jeong ◽  
Yeongyu Moon ◽  
Jungil Choi ◽  
Jeong Doo Heo ◽  
...  

Rearranged during transfection (RET), a receptor tyrosine kinase, is activated by glial cell line-derived neurotrophic factor family ligands. Chromosomal rearrangement or point mutations in RET are observed in patients with papillary thyroid and medullary thyroid carcinomas. Oncogenic alteration of RET results in constitutive activation of RET activity. Therefore, inhibiting RET activity has become a target in thyroid cancer therapy. Here, the anti-tumor activity of a novel RET inhibitor was characterized in medullary thyroid carcinoma cells. The indirubin derivative LDD-2633 was tested for RET kinase inhibitory activity. In vitro, LDD-2633 showed potent inhibition of RET kinase activity, with an IC50 of 4.42 nM. The growth of TT thyroid carcinoma cells harboring an RET mutation was suppressed by LDD-2633 treatment via the proliferation suppression and the induction of apoptosis. The effects of LDD-2633 on the RET signaling pathway were examined; LDD-2633 inhibited the phosphorylation of the RET protein and the downstream molecules Shc and ERK1/2. Oral administration of 20 or 40 mg/kg of LDD-2633 induced dose-dependent suppression of TT cell xenograft tumor growth. The in vivo and in vitro experimental results supported the potential use of LDD-2633 as an anticancer drug for thyroid cancers.


2014 ◽  
Vol 10 (5) ◽  
pp. e901-e904 ◽  
Author(s):  
Silvia Rizzitelli ◽  
Pierangela Giustetto ◽  
Cinzia Boffa ◽  
Daniela Delli Castelli ◽  
Juan Carlos Cutrin ◽  
...  

Author(s):  
Dumitru A Iacobas

Publically available (own) transcriptomic data were re-analyzed to quantify the alteration of functional pathways in the thyroid cancer, establish the gene hierarchy, identify potential gene targets and predict the effects of their manipulation. The expression data were generated from one case of papillary thyroid carcinoma (PTC) and from genetically manipulated BCPAP (papillary) and 8505C (anaplastic) human thyroid cancer cell lines. The study used the genomic fabric perspective that considers the transcriptome as a multi-dimensional mathematical object based on the three independent characteristics that can be derived for each gene from the expression data. We found remarkable remodeling of the thyroid hormone synthesis, cell cycle, oxidative phosphorylation and apoptosis pathways. Serine peptidase inhibitor, Kunitz type, 2 (SPINT2) was identified as the Gene Master Regulator of the investigated PTC. The substantial increase of the expression synergism of SPINT2 with apoptosis genes in the cancer nodule with respect to the surrounding normal tissue (NOR) suggests that its experimental overexpression may force the PTC cells into apoptosis with negligible effect on the NOR cells. The predictive value of the expression coordination for the expression regulation was validated with data from 8505C and BCPAP cells before and after lentiviral transfection with DDX19B.


2017 ◽  
Vol 58 (1) ◽  
pp. 15-23 ◽  
Author(s):  
Chen-Tian Shen ◽  
Wei-Jun Wei ◽  
Zhong-Ling Qiu ◽  
Hong-Jun Song ◽  
Xin-Yun Zhang ◽  
...  

More aggressive thyroid cancer cells show a higher activity of glycometabolism. Targeting cancer cell metabolism has emerged as a novel approach to prevent or treat malignant tumors. Glucose metabolism regulation effect of metformin in papillary thyroid cancer was investigated in the current study. Human papillary thyroid carcinoma (PTC) cell lines BCPAP and KTC1 were used. Cell viability was detected by CCK8 assay. Glucose uptake and relative gene expression were measured in metformin (0–10 mM for 48 h)-treated cells by 18F-FDG uptake assay and western blotting analysis, respectively. MicroPET/CT imaging was performed to detect 18F-FDG uptake in vivo. After treatment with metformin at 0, 2.5, 5 and 10 mM for 48 h, the ratio of p-AMPK to total AMPK showed significant rising in a dose-dependent manner in both BCPAP and KTC1, whereas p-AKT and p-mTOR expression level were downregulated. 18F-FDG uptake reduced after metformin treatment in a dose-dependent manner, corresponding to the reduced expression level of HK2 and GLUT1 in vitro. Xenograft model of PTC using BCPAP cells was achieved successfully. MicroPET/CT imaging showed that in vivo 18F-FDG uptake decreased after treatment with metformin. Immunohistochemistry staining further confirmed the reduction of HK2 and GLUT1 expression in the tumor tissue of metformin-treated PTC xenograft model. In conclusion, metformin could reduce glucose metabolism of PTC in vitro and in vivo. Metformin, by targeting glycometabolism of cancer cells, could be a promising adjuvant therapy alternative in the treatment modality of advanced thyroid carcinoma.


Thyroid ◽  
2000 ◽  
Vol 10 (11) ◽  
pp. 939-943 ◽  
Author(s):  
Jan W.A. Smit ◽  
Janny P. Schröder-van der Elst ◽  
Marcel Karperien ◽  
Ivo Que ◽  
Gabri van der Pluijm ◽  
...  

2017 ◽  
Vol 43 (4) ◽  
pp. 1325-1336 ◽  
Author(s):  
Junyi  Wang ◽  
Haiou Yang ◽  
Yiran Si ◽  
Dongzhi Hu ◽  
Yang Yu ◽  
...  

Background/Aims: Iodine may trigger tumorigenesis and development of thyroid carcinoma, but the mechanisms involved remained elusive. MicroRNA (MiRNAs) are known to be involved in each stage of cancer development; however, the role of miRNAs in iodine-induced tumorigenesis of thyroid carcinoma remained unknown. In this study, we aimed at investigating miRNA related signaling pathway in thyroid cancer cells. Methods: Levels of miRNAs and mRNAs were determined using RT-qPCR and proteins were quantified by western blotting. Cell migration and proliferation were checked using Transwell assay and CCK8 assay respectively. Tumor xenografts in nude mice were established by subcutaneous injection of cancer cells. Results: Mitogen activated protein kinase 1 (MAPK1) was significantly up-regulated, while miR-422a was down-regulated in thyroid cancer cells cultured with high iodine; miR-422a directly bound to the 3’UTR of MAPK1 mRNA. Moreover, miR-422a negatively regulated MAPK1 expression, and down-regulated miR-422a promoted proliferation and migration of TPC-1 cells. In vivo studies also confirmed that iodine promoted tumor growth by suppressing miR-422a and up-regulating MAPK1. Conclusions: Our study illustrates a new pathway comprising iodine, miRNA and MAPK1, and defines a novel mechanism in thyroid cancer.


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