scholarly journals Liposomal Delivery of miR-34b-5p Induced Cancer Cell Death in Thyroid Carcinoma

Cells ◽  
2018 ◽  
Vol 7 (12) ◽  
pp. 265 ◽  
Author(s):  
Hamidreza Maroof ◽  
Farhadul Islam ◽  
LanFeng Dong ◽  
Prabha Ajjikuttira ◽  
Vinod Gopalan ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Cell Cycle Progression ◽  
Cationic Liposome ◽  
Anaplastic Thyroid Carcinoma ◽  
Targeting Therapy ◽  
Functional Roles ◽  
In Vivo Experiments ◽  
Freeze Dried

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.

scholarly journals PARP inhibitor olaparib increases the oncolytic activity of dl922-947 in in vitro and in vivo model of anaplastic thyroid carcinoma

2014 ◽  
Vol 9 (1) ◽  
pp. 78-92 ◽  
Author(s):  
Carmela Passaro ◽  
Massimiliano Volpe ◽  
Ginevra Botta ◽  
Eloise Scamardella ◽  
Giuseppe Perruolo ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Parp Inhibitor ◽  
Anaplastic Thyroid Carcinoma ◽  
In Vivo Model ◽  
Oncolytic Activity

miR-199a-5p suppresses epithelial- mesenchymal-transition in anaplastic thyroid carcinoma cells via targeting Snail signals

2020 ◽  
Vol 29 (3) ◽  
pp. 317-326
Author(s):  
Fengyun Hao ◽  
Ya-Nan Bi ◽  
Lei Wang ◽  
Yubing Wang ◽  
Jilei Ma ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Anaplastic Thyroid Carcinoma ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Novel Approach ◽  
Accurate Expression

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.

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
Keyword(s):  
Thyroid Carcinoma ◽  
Tumor Growth ◽  
Anaplastic Thyroid Carcinoma ◽  
Notch1 Signaling

scholarly journals Novel Long Noncoding RNA miR205HG Functions as an Esophageal Tumor-Suppressive Hedgehog Inhibitor

Cancers ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1707
Author(s):  
Jee Hoon Song ◽  
Alan H. Tieu ◽  
Yulan Cheng ◽  
Ke Ma ◽  
Venkata S. Akshintala ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Noncoding Rna ◽  
Cell Cycle Progression ◽  
Esophageal Tumor ◽  
Cycle Progression ◽  
In Vivo Experiments ◽  
Hh Signaling

Barrett’s esophagus (BE) is a precursor to esophageal adenocarcinoma (EAC). Recently, long noncoding RNAs (lncRNAs) have been identified as key regulators of biological pathways. However, involvement of lncRNAs in the development of BE and EAC has not been well-studied. The aims of the current study were: (1) to study involvement of the lncRNA, miR205HG, in the development of BE and EAC; (2) to clarify the role of miR205HG in in vitro and in vivo experiments; and (3) to investigate the mechanism of miR205HG involving the Hedgehog (Hh) signaling pathway. These experiments revealed that miR205HG was downregulated in EAC vs. normal esophageal epithelia (NE) as well as in EAC cell lines, and its forced overexpression inhibited EAC cell proliferation and cell cycle progression in vitro. Similarly, overexpression of miR205HG inhibited xenograft tumor growth in mice In vivo. Finally, we show that one mechanism of action of miR205HG involves the Hh signaling pathway: miR205HG and Hh expression levels were inversely correlated in both EAC (r = −0.73) and BE (r = −0.83) tissues, and in vitro studies revealed details of Hh signaling inhibition induced by miR205HG. In conclusion, these findings establish that lncRNA miR205HG functions as a tumor suppressor in the development of BE and EAC, at least in part through its effect on the Hh signaling pathway.

scholarly journals Gold-Based Nanoplataform for the Treatment of Anaplastic Thyroid Carcinoma: A Step Forward

Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1242
Author(s):  
Mariana Amaral ◽  
Adília J. Charmier ◽  
Ricardo A. Afonso ◽  
José Catarino ◽  
Pedro Faísca ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Cell Viability ◽  
Near Infrared ◽  
Anaplastic Thyroid Carcinoma ◽  
Infrared Light ◽  
Surface Plasmon Resonances ◽  
Plasmon Resonances ◽  
Near Future

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.

scholarly journals Down-regulated HSDL2 expression suppresses cell proliferation and promotes apoptosis in papillary thyroid carcinoma

2019 ◽  
Vol 39 (6) ◽  
Author(s):  
Jing Zeng ◽  
Xiao Ma ◽  
Jinjing Wang ◽  
Ran Liu ◽  
Yun Shao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Target Genes ◽  
Mrna Level ◽  
Papillary Thyroid ◽  
Bioinformatics Analyses ◽  
In Vivo Experiments

Abstract Papillary thyroid carcinoma (PTC) is the most common type of thyroid cancer. Hydroxysteroid dehydrogenase like 2 (HSDL2) can regulate lipid metabolism and take part in cell proliferation. The purpose of the present study was to explore functional role of HSDL2 gene in PTC. The expression of HSDL2 protein in PTC tissues was estimated using immunohistochemistry analysis (IHC). HSDL2 mRNA level was detected through quantitative real-time polymerase chain reaction (qRT-PCR). Effects of HSDL2 gene on cell proliferation and apoptosis were assessed using the shRNA method for both in vitro and in vivo experiments. Potential target genes of HSDL2 were determined via bioinformatics analyses and Western blotting. HSDL2 was up-regulated in PTC tissues and cell lines compared with the controls (all P<0.05). Inhibiting HSDL expression could suppress PTC cell proliferation and cycle, and promote apoptosis in vitro. In vivo, the knockdown of HSDL2 gene could significantly suppress tumor growth (all P<0.05). Furthermore, AKT3, NFATc2 and PPP3CA genes might be potential targets of HSDL2 in PTC. HSDL2 expression was increased in PTC tissues and cells, which could promote tumor progression in vitro and in vivo.

scholarly journals Chidamide combined with doxorubicin leads to synergistic anti-cancer effect and induces autophagy through inhibiting the PI3K/Akt/mTOR pathway in anaplastic thyroid carcinoma

2020 ◽  
Author(s):  
Yishan He ◽  
Xinguang Qiu
Keyword(s):  
Thyroid Carcinoma ◽  
Cell Lines ◽  
Treatment Strategies ◽  
Inhibitory Effect ◽  
Anaplastic Thyroid Carcinoma ◽  
Tor Signaling ◽  
Invasion And Migration ◽  
Anti Cancer

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.

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