scholarly journals Chrysin activates Notch1 signaling and suppresses tumor growth of anaplastic thyroid carcinoma in vitro and in vivo

Cancer ◽  
2012 ◽  
Vol 119 (4) ◽  
pp. 774-781 ◽  
Author(s):  
Xiao-Min Yu ◽  
TramAnh Phan ◽  
Priyesh N. Patel ◽  
Renata Jaskula-Sztul ◽  
Herbert Chen
2014 ◽  
Vol 9 (1) ◽  
pp. 78-92 ◽  
Author(s):  
Carmela Passaro ◽  
Massimiliano Volpe ◽  
Ginevra Botta ◽  
Eloise Scamardella ◽  
Giuseppe Perruolo ◽  
...  

2020 ◽  
Vol 29 (3) ◽  
pp. 317-326
Author(s):  
Fengyun Hao ◽  
Ya-Nan Bi ◽  
Lei Wang ◽  
Yubing Wang ◽  
Jilei Ma ◽  
...  

MicroRNAs (miRNAs) have been validated to play prominent roles in the occurrence and development of anaplastic thyroid carcinoma (ATC). miR-199a-5p was previously reported to act as a tumor suppressor or oncomiRNA in various types of cancer. However, its accurate expression, function, and mechanism in ATC remain unclear. Here, we find that miR-199a-5p is significantly downregulated in ATC tissues compared with adjacent non-cancerous tissues. Overexpression of miR-199a-5p significantly inhibits migration and invasion of ATC cells in vitro, and lung metastasis in vivo. Importantly, miR-199a-5p suppresses epithelial-mesenchymal transition (EMT) both in vitro and in vivo by targeting Snail. Taken together, this study reveals that miR-199a-5p is critical to the EMT progression in ATC cells. Targeting the pathway described here may be a novel approach for inhibiting metastasis of ATC.


Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1242
Author(s):  
Mariana Amaral ◽  
Adília J. Charmier ◽  
Ricardo A. Afonso ◽  
José Catarino ◽  
Pedro Faísca ◽  
...  

Anaplastic thyroid carcinoma (ATC) is a very rare subtype of thyroid carcinoma and one of the most lethal malignancies. Poor prognosis is mainly associated with its undifferentiated nature, inoperability, and failing to respond to the typically used therapies for thyroid cancer. Photothermal Therapy (PTT) entails using light to increase tissues’ temperature, leading to hyperthermia-mediated cell death. Tumours are more susceptible to heat as they are unable to dissipate it. By using functionalized gold nanoparticles (AuNPs) that transform light energy into heat, it is possible to target the heat to the tumour. This study aims to formulate ATC-targeted AuNPs able to convert near-infrared light into heat, for PTT of ATC. Different AuNPs were synthetized and coated. Size, morphology, and surface plasmon resonances band were determined. The optimized coated-AuNPs were then functionalized with ligands to assess ATC’s specificity. Safety, efficacy, and selectivity were assessed in vitro. The formulations were deemed safe when not irradiated (>70% cell viability) and selective for ATC. However, when irradiated, holo-transferrin-AuNPs were the most cytotoxic (22% of cell viability). The biodistribution and safety of this formulation was assessed in vivo. Overall, this novel formulation appears to be a highly promising approach to evaluate in a very near future.


2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Qin Chen ◽  
Wen-Ying Yu ◽  
Huan-Huan Zhang ◽  
Song-Zhao Zhang ◽  
Jie Fang ◽  
...  

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.


2020 ◽  
Author(s):  
Yishan He ◽  
Xinguang Qiu

AbstractAnaplastic thyroid carcinoma (ATC) is a fatal malignant tumor, which belongs to the thyroid cancer with an overwhelmingly poor prognosis and eagerly demands effective systemic treatment strategies. We aimed to investigate the antitumor characteristics of Chidamide (CS055) in combination with doxorubicin (Dox) on ATC, and explore the underlying molecular mechanism. Herein, we found that CS055 and Dox inhibited proliferation, invasion and migration and promoted apoptosis of ATC cells. CS055 and Dox induced autophagic cell death (ADC) of ATC cell lines. And the expression of autophagy markers, BECN1, Atg5 and LC3-II was significantly enhanced in ATC cell lines treated with CS055 and Dox. Similarly, the in vivo study showed that CS055 and Dox administration significantly reduced tumor growth and induced tumor cell autophagy. Interestingly, the synergistic anti-cancer effect of CS055 in combination with doxorubicin was observed in vitro and in vivo. In addition, CS055 and Dox suppressed the proteins expression of p-P13K, p-AKT and mTOR in vitro and in vivo and combination of CS055 and Dox exhibited greatest inhibitory effect. Taken together, our findings concluded that CS055 in combination with Dox exerted antitumor activities and triggered autophogy in thyroid carcinoma probably through inhibiting the P13K/AKT/m/TOR signaling pathway.


2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Manoj Garg ◽  
Deepika Kanojia ◽  
Anand Mayakonda ◽  
Trivadi S Ganesan ◽  
Bindhya Sadhanandhan ◽  
...  

Cells ◽  
2018 ◽  
Vol 7 (12) ◽  
pp. 265 ◽  
Author(s):  
Hamidreza Maroof ◽  
Farhadul Islam ◽  
LanFeng Dong ◽  
Prabha Ajjikuttira ◽  
Vinod Gopalan ◽  
...  

This study aims to determine the functional roles of microRNA-34b-5p (miR-34b) in the suppression of anaplastic thyroid carcinoma. We used hydration-of-freeze-dried-matrix (HFDM) formulated liposomes (liposome-loaded miR-34b) for effective delivery of miR-34b to anaplastic thyroid carcinoma in vitro and in vivo. Real time polymerase chain was used to determine the level of miR-34b. Immunocytochemistry, Western blot and ELISA were carried out to determine the effect of this manipulation on VEGF-A expression. In addition, an in vivo xenotransplantation mouse model was used to investigate the functional roles of overexpression of miR-34b in the carcinoma. In anaplastic thyroid carcinoma cells, miR-34b expression was low and significant overexpression (p < 0.05) was noted following transfection with liposome-loaded miR-34b. The miR-34b overexpressed thyroid carcinoma cell lines showed reduction in VEGF-A protein expression, decreased cell proliferation, decreased wound healing, reduced cell cycle progression and increased apoptosis (p < 0.05). In in vivo experiments, when compared to control groups, smaller tumours formed upon intravenous administration of liposome-loaded miR-34b. To conclude, the current study confirmed the tumour suppressor properties of miR-34b via VEGF-A regulation in anaplastic thyroid carcinoma. In addition, delivery of miR-34b using cationic liposome could be a useful therapeutic strategy for targeting therapy in the carcinoma.


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