BMP-7-Induced Cell Cycle Arrest of Anaplastic Thyroid Carcinoma Cells via p21CIP1 and p27KIP1

2001 ◽  
Vol 285 (3) ◽  
pp. 773-781 ◽  
Author(s):  
Åsa Franzén ◽  
Nils-Erik Heldin
Keyword(s):  
Cell Cycle ◽  
Thyroid Carcinoma ◽  
Cell Cycle Arrest ◽  
Anaplastic Thyroid Carcinoma ◽  
Carcinoma Cells ◽  
Cycle Arrest

scholarly journals HDAC1 and HDAC2 Double Knockout Triggers Cell Apoptosis in Advanced Thyroid Cancer

2019 ◽  
Vol 20 (2) ◽  
pp. 454 ◽  
Author(s):  
Ching-Ling Lin ◽  
Ming-Lin Tsai ◽  
Chun-Yu Lin ◽  
Kai-Wen Hsu ◽  
Wen-Shyang Hsieh ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Thyroid Cancer ◽  
Thyroid Carcinoma ◽  
Histone Acetylation ◽  
Cell Cycle Arrest ◽  
Cell Apoptosis ◽  
Anaplastic Thyroid Carcinoma ◽  
Double Knockout ◽  
Cycle Arrest ◽  
Advanced Thyroid Cancer

Anaplastic thyroid carcinoma (ATC) and squamous thyroid carcinoma (STC) are both rare and advanced thyroid malignancies with a very poor prognosis and an average median survival time of 5 months and less than 20% of affected patients are alive 1 year after diagnosis. The clinical management of both ATC and STC is very similar because they are not particularly responsive to radiotherapy and chemotherapy. This inspired us to explore a novel and effective clinically approved therapy for ATC treatment. Histone deacetylase inhibitor (HDACi) drugs are recently FDA-approved drug for malignancies, especially for blood cell cancers. Therefore, we investigated whether an HDACi drug acts as an effective anticancer drug for advanced thyroid cancers. Cell viability analysis of panobinostat treatment demonstrated a significant IC50 of 0.075 µM on SW579 STC cells. In addition, panobinostat exposure activated histone acetylation and triggered cell death mainly through cell cycle arrest and apoptosis-related protein activation. Using CRISPR/Cas9 to knock out HDAC1 and HDAC2 genes in SW579 cells, we observed that the histone acetylation level and cell cycle arrest were enhanced without any impact on cell growth. Furthermore, HDAC1 and HDAC2 double knockout (KO) cells showed dramatic cell apoptosis activation compared to HDAC1 and HDAC2 individual KO cells. This suggests expressional and biofunctional compensation between HDAC1 and HDAC2 on SW579 cells. This study provides strong evidence that panobinostat can potentially be used in the clinic of advanced thyroid cancer patients.

Diallyl trisulfide induces G2/M cell-cycle arrest and apoptosis in anaplastic thyroid carcinoma 8505C cells

2019 ◽  
Vol 10 (11) ◽  
pp. 7253-7261
Author(s):  
Jiangxia Zheng ◽  
Xian Cheng ◽  
Shichen Xu ◽  
Li Zhang ◽  
Jie Pan ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Thyroid Carcinoma ◽  
Cell Cycle Arrest ◽  
Signaling Pathway ◽  
Anaplastic Thyroid Carcinoma ◽  
Diallyl Trisulfide ◽  
M Cell ◽  
Cycle Arrest

DATS induces G2/M cell-cycle arrest and apoptosis through ATM-Chk1-Cdc25C signaling pathway in ATC 8505C cells.

Synergistic Effect of α-Solanine and Cisplatin Induces Apoptosis and Enhances Cell Cycle Arrest in Human Hepatocellular Carcinoma Cells

2020 ◽  
Vol 19 (18) ◽  
pp. 2197-2210 ◽  
Author(s):  
Sherien M. El-Daly ◽  
Shaimaa A. Gouhar ◽  
Amira M. Gamal-Eldeen ◽  
Fatma F. Abdel Hamid ◽  
Magdi N. Ashour ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Synergistic Effect ◽  
Cell Cycle Arrest ◽  
Combination Treatment ◽  
Carcinoma Cells ◽  
Cell Growth Inhibition ◽  
Cycle Arrest ◽  
Induced Apoptosis ◽  
Human Hepatocellular Carcinoma Cells

Aim: The clinical application of cisplatin is limited by severe side effects associated with high applied doses. The synergistic effect of a combination treatment of a low dose of cisplatin with the natural alkaloid α-solanine on human hepatocellular carcinoma cells was evaluated. Methods: HepG2 cells were exposed to low doses of α-solanine and cisplatin, either independently or in combination. The efficiency of this treatment modality was evaluated by investigating cell growth inhibition, cell cycle arrest, and apoptosis enhancement. Results: α-solanine synergistically potentiated the effect of cisplatin on cell growth inhibition and significantly induced apoptosis. This synergistic effect was mediated by inducing cell cycle arrest at the G2/M phase, enhancing DNA fragmentation and increasing apoptosis through the activation of caspase 3/7 and/or elevating the expression of the death receptors DR4 and DR5. The induced apoptosis from this combination treatment was also mediated by reducing the expression of the anti-apoptotic mediators Bcl-2 and survivin, as well as by modulating the miR-21 expression. Conclusion: Our study provides strong evidence that a combination treatment of low doses of α-solanine and cisplatin exerts a synergistic anticancer effect and provides an effective treatment strategy against hepatocellular carcinoma.

Trichosanthes dioica seed lectin inhibits Ehrlich ascites carcinoma cells growth in vivo in mice by inducing G 0 /G 1 cell cycle arrest

2021 ◽  
Author(s):  
Shaikh Shohidul Islam ◽  
Md. Rezaul Karim ◽  
A. K. M. Asaduzzaman ◽  
A. H. M. Khurshid Alam ◽  
Zahid Hayat Mahmud ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Ehrlich Ascites Carcinoma ◽  
Carcinoma Cells ◽  
Cycle Arrest ◽  
Ehrlich Ascites ◽  
Trichosanthes Dioica
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