scholarly journals Peroxisome Proliferator-activated Receptor Gamma Activation Induces Cell Cycle Arrest via the p53-independent Pathway in Human Anaplastic Thyroid Cancer Cells

2002 ◽  
Vol 93 (12) ◽  
pp. 1358-1365 ◽  
Author(s):  
Sung Hwa Chung ◽  
Naoyoshi Onoda ◽  
Tetsuro Ishikawa ◽  
Kana Ogisawa ◽  
Chiemi Takenaka ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Thyroid Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Anaplastic Thyroid Cancer ◽  
Peroxisome Proliferator ◽  
Gamma Activation ◽  
Peroxisome Proliferator Activated Receptor ◽  
Cycle Arrest ◽  
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 Selenite Induces Cell Cycle Arrest and Apoptosis via Reactive Oxygen Species-Dependent Inhibition of the AKT/mTOR Pathway in Thyroid Cancer

2021 ◽  
Vol 11 ◽  
Author(s):  
Zhen Cheng ◽  
Shuang Yu ◽  
Weiman He ◽  
Jie Li ◽  
Tianyi Xu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Thyroid Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Sodium Selenite ◽  
Oxygen Species ◽  
Cycle Arrest ◽  
Intracellular Ros ◽  
Thyroid Cancer Cells

Thyroid cancer is the most common endocrine malignancy, and its incidence has increased in the past decades. Selenium has been shown to have therapeutic effects against several tumors. However, its role in thyroid cancer and its underlying molecular mechanism remains to be explored. In the present study, we demonstrated that sodium selenite significantly decreased cell viability and induced G0/G1 cell cycle arrest and apoptosis in thyroid cancer cells in a dose-dependent manner. Transcriptomics revealed that sodium selenite induced intracellular reactive oxygen species (ROS) by promoting oxidative phosphorylation. Increased intracellular ROS levels inhibited the AKT/mTOR signaling pathway and upregulated EIF4EBP3. Intracellular ROS inhibition by N-acetylcysteine (NAC) ameliorated the cellular effects of sodium selenite. The in vitro findings were reproduced in xenograft thyroid tumor models. Our data demonstrated that sodium selenite exhibits strong anticancer effects against thyroid cancer cells, which involved ROS-mediated inhibition of the AKT/mTOR pathway. This suggests that sodium selenite may serve as a therapeutic option for advanced thyroid cancer.

scholarly journals Valproic Acid Induces Apoptosis and Cell Cycle Arrest in Poorly Differentiated Thyroid Cancer Cells

2005 ◽  
Vol 90 (3) ◽  
pp. 1383-1389 ◽  
Author(s):  
Maria G. Catalano ◽  
Nicoletta Fortunati ◽  
Mariateresa Pugliese ◽  
Lucia Costantino ◽  
Roberta Poli ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Valproic Acid ◽  
Thyroid Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Differentiated Thyroid Cancer ◽  
Cycle Arrest ◽  
Poorly Differentiated ◽  
Thyroid Cancer Cells

scholarly journals Heme Oxygenase-1 Inhibitors Induce Cell Cycle Arrest and Suppress Tumor Growth in Thyroid Cancer Cells

2018 ◽  
Vol 19 (9) ◽  
pp. 2502 ◽  
Author(s):  
Po-Sheng Yang ◽  
Yi-Chiung Hsu ◽  
Jie-Jen Lee ◽  
Ming-Jen Chen ◽  
Shih-Yuan Huang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Thyroid Cancer ◽  
Cyclin D1 ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1 ◽  
G1 Arrest ◽  
Cycle Arrest ◽  
Thyroid Cancer Cells

Heme oxygenase-1 (HO-1) is induced by a variety of stimuli and plays a multifaceted role in cellular protection. We have shown that HO-1 is overexpressed in thyroid cancer and is associated with tumor aggressiveness. Therefore, we set out to assess the effects of HO-1 inhibitors on the biology of thyroid cancer cells. Two different classes of HO-1 inhibitors were used, including a metalloporphyrin, zinc protoporphyrin-IX (ZnPP), and an azole antifungal agent, ketoconazole. The viability and colony formation of thyroid cancer cells decreased in a concentration- and time-dependent fashion following treatment with HO-1 inhibitors. Cancer cells exhibited a higher sensitivity to HO-1 inhibitors than non-malignant cells. HO-1 inhibitors induced a G0/G1 arrest accompanied by decreased cyclin D1 and CDK4 expressions and an increase in levels of p21 and p27. HO-1 inhibitors significantly increased intracellular ROS levels and suppressed cell migration and invasion. Oxygen consumption rate and mitochondrial mass were increased with ZnPP treatment. Mice treated with ZnPP had a reduced xenograft growth and diminished cyclin D1 and Ki-67 staining in tumor sections. Taken together, HO-1 inhibitors might have therapeutic potential for inducing cell cycle arrest and promoting growth suppression of thyroid cancer cells in vitro and in vivo.

scholarly journals Lenvatinib Promotes the Antitumor Effects of Doxorubicin in Anaplastic Thyroid Cancer

2020 ◽  
Author(s):  
Xi Su ◽  
Jiaxin Liu ◽  
Haihong Zhang ◽  
Qingqing Gu ◽  
Xinrui Zhou ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Thyroid Cancer ◽  
Combination Therapy ◽  
Cell Cycle Arrest ◽  
Anaplastic Thyroid Cancer ◽  
Antitumor Efficacy ◽  
Potential Candidate ◽  
Antitumor Effects ◽  
Cycle Arrest

Abstract Background Anaplastic thyroid cancer (ATC) is a kind of rare thyroid cancer with very poor prognosis. It is one of the deadliest cancers in human due to the aggressive behavior and resistance to treatment. Doxorubicin has been approved in ATC treatment as a single agent, but monotherapy still shows no improvement of the total survival in advanced ATC. Lenvatinib was investigated with encouraging results in treating the patients with radioiodine-refractory differentiated thyroid cancer (DTC). However, antitumor efficacy of combination therapy with lenvatinib and doxorubicin remains largely unclear. Methods The antitumor efficacy of combination therapy with lenvatinib and doxorubicin on ATC cell proliferation and was assessed by the MTT assay and colony formation. Flow cytometry were employed to assess ATC cells’ apoptosis and cell cycle arrest in response to combination therapy. Xenograft models were used to test its in vivo antitumor activity. Result Lenvatinib monotherapy was less effective than doxorubicin in treating ATC cell lines and xenografts model. The combination therapy of lenvatinib and doxorubicin significantly inhibited ATC cell proliferation and tumor growth in nude mice, and induced cell apoptosis and cell cycle arrest in compared to lenvatinib or doxorubicin monotherapy. Conclusion Lenvatinib promotes the antitumor effects of doxorubicin in ATC cell and xenografts model. Lenvatinib/doxorubicin combination may be a potential candidate therapeutic approach for ATC.

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