The Effect of the Combined Action of Roscovitine and Paclitaxel on the Apoptotic and Cell Cycle Regulatory Mechanisms in Colon and Anaplastic Thyroid Cancer Cells

2013 ◽  
Author(s):  
Vladimir Pushkarev ◽  
O. I. Kovzun ◽  
V. M. Pushkarev ◽  
M. D. Tronko
Keyword(s):  
Cell Cycle ◽  
Thyroid Cancer ◽  
Cancer Cells ◽  
Anaplastic Thyroid Cancer ◽  
Regulatory Mechanisms ◽  
Combined Action ◽  
Thyroid Cancer Cells

scholarly journals The Effect of the Combined Action of Roscovitine and Paclitaxel on the Apoptotic and Cell Cycle Regulatory Mechanisms in Colon and Anaplastic Thyroid Cancer Cells

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
V. V. Pushkarev ◽  
O. I. Kovzun ◽  
V. M. Pushkarev ◽  
M. D. Tronko
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Anaplastic Thyroid Cancer ◽  
Cyclin Dependent Kinases ◽  
New Therapeutic Approaches ◽  
Drug Concentrations ◽  
Preclinical Trials ◽  
Combined Action ◽  
Undifferentiated Thyroid Cancer ◽  
Thyroid Cancer Cells

Aim. To study the significance of cyclin-dependent kinases (Cdks) in paclitaxel-dependent apoptosis in colon and undifferentiated thyroid cancer cells. Materials and Methods. Experiments were performed on undifferentiated thyroid carcinoma (KTC-2) and colon carcinoma (ARO) cell lines. Cells were treated with paclitaxel (Ptx) and inhibitor of Cdk, roscovitine. Cell survival test and Western blotting were used for characterization of the effects of paclitaxel and roscovitine on cancer cells. Results. It was shown that not c-Jun N-terminal kinase, but cyclin-dependent kinases are responsible for antiapoptotic Bcl-2 phosphorylation. Cdk inhibition enhanced the cytotoxic effects of Ptx at low drug concentrations. There was antagonism between Ptx and roscovitine at higher (25 nM) paclitaxel concentrations. Conclusion. Using of paclitaxel at low (2.5 to 5 nM) concentrations and roscovitine is a promising combination for further preclinical trials for the development of new therapeutic approaches to the treatment of colon and anaplastic thyroid cancer.

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.

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.

scholarly journals Biochemical effects of combined action of ?-irradiation and paclitaxel on anaplastic thyroid cancer cells

2013 ◽  
Vol 85 (1) ◽  
pp. 51-61
Author(s):  
V. M. Pushkarev ◽  
◽  
O. I. Kovzun ◽  
V. V. Pushkarev ◽  
M. D. Tronko ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Anaplastic Thyroid Cancer ◽  
Biochemical Effects ◽  
Combined Action ◽  
Thyroid Cancer Cells

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

scholarly journals Synergistic anti-proliferative effect of metformin and sorafenib on growth of anaplastic thyroid cancer cells and their stem cells

2015 ◽  
Vol 33 (4) ◽  
pp. 1994-2000 ◽  
Author(s):  
GUOFANG CHEN ◽  
DIANA NICULA ◽  
KOSTJA RENKO ◽  
MICHAEL DERWAHL
Keyword(s):  
Stem Cells ◽  
Thyroid Cancer ◽  
Cancer Cells ◽  
Anaplastic Thyroid Cancer ◽  
Proliferative Effect ◽  
Thyroid Cancer Cells

scholarly journals ZIC1 Is a Putative Tumor Suppressor in Thyroid Cancer by Modulating Major Signaling Pathways and Transcription Factor FOXO3a

2014 ◽  
Vol 99 (7) ◽  
pp. E1163-E1172 ◽  
Author(s):  
Wei Qiang ◽  
Yuan Zhao ◽  
Qi Yang ◽  
Wei Liu ◽  
Haixia Guan ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Transcription Factor ◽  
Thyroid Cancer ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Colony Formation ◽  
Promoter Hypermethylation ◽  
Migration And Invasion ◽  
Thyroid Cancer Cells

Context: ZIC1 has been reported to be overexpressed and plays an oncogenic role in some brain tumors, whereas it is inactivated by promoter hypermethylation and acts as a tumor suppressor in gastric and colorectal cancers. However, until now, its biological role in thyroid cancer remains totally unknown. Objectives: The aim of this study is to explore the biological functions and related molecular mechanism of ZIC1 in thyroid carcinogenesis. Setting and Design: Quantitative RT-PCR (qRT-PCR) was performed to evaluate mRNA expression of investigated genes. Methylation-specific PCR was used to analyze promoter methylation of the ZIC1 gene. The functions of ectopic ZIC1 expression in thyroid cancer cells were determined by cell proliferation and colony formation, cell cycle and apoptosis, as well as cell migration and invasion assays. Results: ZIC1 was frequently down-regulated by promoter hypermethylation in both primary thyroid cancer tissues and thyroid cancer cell lines. Moreover, our data showed that ZIC1 hypermethylation was significantly associated with lymph node metastasis in patients with papillary thyroid cancer. Notably, restoration of ZIC1 expression in thyroid cancer cells dramatically inhibited cell proliferation, colony formation, migration and invasion, and induced cell cycle arrest and apoptosis by blocking the activities of the phosphatidylinositol-3-kinase (PI3K)/Akt and RAS/RAF/MEK/ERK (MAPK) pathways, and enhancing FOXO3a transcriptional activity. Conclusions: Our data demonstrate that ZIC1 is frequently inactivated by promoter hypermethyaltion and functions as a tumor suppressor in thyroid cancer through modulating PI3K/Akt and MAPK signaling pathways and transcription factor FOXO3a.

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