scholarly journals High Iodine Induces the Proliferation of Papillary and Anaplastic Thyroid Cancer Cells via AKT/Wee1/CDK1 Axis

2021 ◽  
Vol 11 ◽  
Author(s):  
Chunpeng Lv ◽  
Yanhui Gao ◽  
Jinyin Yao ◽  
Yan Li ◽  
Qun Lou ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Thyroid Cancer ◽  
Cancer Cells ◽  
Cell Cycle Progression ◽  
Anaplastic Thyroid Cancer ◽  
Underlying Mechanism ◽  
High Iodine ◽  
Akt Phosphorylation ◽  
Thyroid Cancer Cells

High iodine can alter the proliferative activity of thyroid cancer cells, but the underlying mechanism has not been fully elucidated. Here, the role of high iodine in the proliferation of thyroid cancer cells was studied. In this study, we demonstrated that high iodine induced the proliferation of BCPAP and 8305C cells via accelerating cell cycle progression. The transcriptome analysis showed that there were 295 differentially expressed genes (DEGs) in BCPAP and 8305C cells induced by high iodine, among which CDK1 expression associated with the proliferation of thyroid cancer cells induced by high iodine. Moreover, the western blot analysis revealed that cells exposed to high iodine enhanced the phosphorylation activation of AKT and the expression of phospho-Wee1 (Ser642), while decreasing the expression of phospho-CDK1 (Tyr15). Importantly, the inhibition of AKT phosphorylation revered the expression of CDK1 induced by high iodine and arrested the cell cycle in the G1 phase, decreasing the proliferation of thyroid cancer cells induced by high iodine. Taken together, these findings suggested that high iodine induced the proliferation of thyroid cancer cells through AKT-mediated Wee1/CDK1 axis, which provided new insights into the regulation of proliferation of thyroid cancer cells by iodine.

scholarly journals miR-32-5p Inhibits the Proliferation, Migration and Invasion of Thyroid Cancer Cells by Regulating Twist1

2021 ◽  
Author(s):  
Qing Liu ◽  
Ouyang Li ◽  
Chi Zhou ◽  
Yu Wang ◽  
Chunxue He ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Transition Process ◽  
Underlying Mechanism ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Thyroid Cancer Cells

Abstract Background: Thyroid cancer is the most prevalent malignancy and one of the leading causes of cancer-related deaths. Recent studies have revealed that microRNAs (miRNAs) play an important role in tumorigenesis in various cancer types by affecting the expression of its targets. However, the role of miR-32-5p in thyroid cancer remains limited. Methods: In this study, we attempt to explore the role of miR-32-5p in thyroid cancer and elucidate the underlying mechanism. Expression of miR-32-5p was determined by quantitative reverse transcription PCR. Functional assays were performed by CCK-8 assay, cell colony assay, cell apoptosis assay, cell migration and invasion assays, cell cycle assay and luciferase assay. Protein expression was analyzed by Western blot.Results: In the present study, the role of miR-32-5p in thyroid cancer was firstly explored. It is found that miR-32-5p was downregulated in thyroid cancer tissues and cells. Overexpression of miR-32-5p inhibited thyroid cancer cells proliferation, migration, invasion and epithelial‐mesenchymal transition process; while suppression of miR-32-5p exhibited an opposite effect on thyroid cancer cells. In addition, In addition, a luciferase assay showed Twist1 was identified as a direct target of miR-32-5p in thyroid cancer, and further study showed that restoration of Twist1 attenuated the biological effect of miR-32-5p on thyroid cancer cells. Conclusion: In conclusion, our results demonstrated miR-32-5p functions as a tumor suppressor by targeting Twist1 in thyroid cancer, providing a novel insight into thyroid cancer therapy.

Role of 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside in the Growth Regulation of Anaplastic Thyroid Cancer Cells Lines

2006 ◽  
Vol 21 (2) ◽  
pp. 125
Author(s):  
Ja Young Song ◽  
Tae Yong Kim ◽  
Won Bae Kim ◽  
Young Kee Shong ◽  
Yoon Soo Rhee ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Growth Regulation ◽  
Anaplastic Thyroid Cancer ◽  
Thyroid Cancer Cells

scholarly journals Oncogenic role of miR-17-92 cluster in anaplastic thyroid cancer cells

2008 ◽  
Vol 99 (6) ◽  
pp. 1147-1154 ◽  
Author(s):  
Shu Takakura ◽  
Norisato Mitsutake ◽  
Masahiro Nakashima ◽  
Hiroyuki Namba ◽  
Vladimir A. Saenko ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Anaplastic Thyroid Cancer ◽  
Thyroid Cancer Cells

Antiproliferative Effects of Cynaropicrin on Anaplastic Thyroid Cancer Cells

2019 ◽  
Vol 19 (1) ◽  
pp. 59-66 ◽  
Author(s):  
Saverio M. Lepore ◽  
Valentina Maggisano ◽  
Giovanni E. Lombardo ◽  
Jessica Maiuolo ◽  
Vincenzo Mollace ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Lipid Peroxidation ◽  
Thyroid Cancer ◽  
Cancer Cells ◽  
Reactive Oxygen ◽  
Anaplastic Thyroid Cancer ◽  
Oxygen Species ◽  
Stat3 Phosphorylation ◽  
Thyroid Cancer Cells

Background: The sesquiterpene lactone cynaropicrin, a major constituent of the artichoke leaves extracts, has shown several biologic activities in many preclinical experimental models, including anti-proliferative effects. Objective: Herein we evaluated the effects of cynaropicrin on the growth of three human anaplastic thyroid carcinoma cell lines, investigating the molecular mechanism underlying its action. Method: MTT assay was used to evaluate the viability of CAL-62, 8505C and SW1736 cells, and flow cytometry to analyse cell cycle distribution. Western blot was performed to detect the levels of STAT3 phosphorylation and NFkB activation. Antioxidant effects were analyzed by measuring the reactive oxygen species and malonyldialdehyde dosage was used to check the presence of lipid peroxidation. Results: Viability of CAL-62, 8505C and SW1736 cells was significantly reduced by cynaropicrin in a dose- and time-dependent way, with an EC50 of about 5 µM observed after 48 h of treatment with the compound. Cellular growth inhibition was accompanied both by an arrest of the cell cycle, mainly in the G2/M phase, and the presence of a significant percentage of necrotic cells. After 48 h of treatment with 10 µM of cynaropicrin, a reduced nuclear expression of NFkB and STAT3 phosphorylation were also revealed. Moreover, we observed an increase in lipid peroxidation, without any significant effect on the reactive oxygen species production. Conclusion: These results demonstrate that cynaropicrin reduces the viability and promotes cytotoxic effects in anaplastic thyroid cancer cells associated with reduced NFkB expression, STAT3 phosphorylation and increased lipid peroxidation. Further characterization of the properties of this natural compound may open the way for using cynaropicrin as an adjuvant in the treatment of thyroid cancer.

Histone Deacetylase Inhibitors Promote Apoptosis and Differential Cell Cycle Arrest in Anaplastic Thyroid Cancer Cells

Thyroid ◽  
2001 ◽  
Vol 11 (4) ◽  
pp. 315-325 ◽  
Author(s):  
Victoria L. Greenberg ◽  
Jennifer M. Williams ◽  
John P. Cogswell ◽  
Michael Mendenhall ◽  
Stephen G. Zimmer
Keyword(s):  
Cell Cycle ◽  
Thyroid Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Histone Deacetylase ◽  
Histone Deacetylase Inhibitors ◽  
Anaplastic Thyroid Cancer ◽  
Cycle Arrest ◽  
Differential Cell ◽  
Thyroid Cancer Cells
Sign in / Sign up

Export Citation Format

Share Document