Role of autophagy in the resistance to tumour necrosis factor-related apoptosis-inducing ligand-induced apoptosis in papillary and anaplastic thyroid cancer cells

Endocrine ◽  
2013 ◽  
Vol 45 (2) ◽  
pp. 256-262 ◽  
Author(s):  
Sang-Man Jin ◽  
Hye Won Jang ◽  
Seo Young Sohn ◽  
Na Kyung Kim ◽  
Ji Young Joung ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Anaplastic Thyroid Cancer ◽  
Induced Apoptosis ◽  
Thyroid Cancer Cells ◽  
Necrosis Factor

scholarly journals Bcl-2-Associated X Protein Is the Main Mediator of Manumycin A-Induced Apoptosis in Anaplastic Thyroid Cancer Cells

2005 ◽  
Vol 90 (6) ◽  
pp. 3583-3591 ◽  
Author(s):  
Jingxuan Pan ◽  
Huizhi Huang ◽  
Lily Sun ◽  
Bingliang Fang ◽  
Sai-Ching Jim Yeung
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Anaplastic Thyroid Cancer ◽  
X Protein ◽  
Induced Apoptosis ◽  
Thyroid Cancer Cells

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

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 CRSP8 promotes thyroid cancer progression by antagonizing IKKα-induced cell differentiation

2020 ◽  
Author(s):  
Yina Liao ◽  
Yijun Hua ◽  
Yizhuo Li ◽  
Changlin Zhang ◽  
Wendan Yu ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Direct Interaction ◽  
Anaplastic Thyroid Cancer ◽  
Human Thyroid ◽  
Induced Apoptosis ◽  
Thyroid Cancer Cells

Abstract CRSP8 plays an important role in recruiting mediators to genes through direct interaction with various DNA-bound transactivators. In this study, we uncovered the unique function of CRSP8 in suppressing thyroid cancer differentiation and promoting thyroid cancer progression via targeting IKKα signaling. CRSP8 was highly expressed in human thyroid cancer cells and tissues, especially in anaplastic thyroid cancer (ATC). Knockdown of CRSP8 suppressed cell growth, migration, invasion, stemness, and induced apoptosis and differentiation in ATC cells, while its overexpression displayed opposite effects in differentiated thyroid cancer (DTC) cells. Mechanistically, CRSP8 downregulated IKKα expression by binding to the IKKα promoter region (−257 to −143) to negatively regulate its transcription. Knockdown or overexpression of IKKα significantly reversed the expression changes of the differentiation and EMT-related markers and cell growth changes mediated by CRSP8 knockdown or overexpression in ATC or DTC cells. The in vivo study also validated that CRSP8 knockdown inhibited the growth of thyroid cancer by upregulating IKKα signaling in a mouse model of human ATC. Furthermore, we found that CRSP8 regulated the sensitivity of thyroid cancer cells to chemotherapeutics, including cisplatin and epirubicin. Collectively, our results demonstrated that CRSP8 functioned as a modulator of IKKα signaling and a suppressor of thyroid cancer differentiation, suggesting a potential therapeutic strategy for ATC by targeting CRSP8/IKKα pathway.

Regulation of tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by DJ-1 in thyroid cancer cells

2008 ◽  
Vol 15 (2) ◽  
pp. 535-544 ◽  
Author(s):  
H.-Y. Zhang ◽  
H.-Q. Wang ◽  
H.-M. Liu ◽  
Y. Guan ◽  
Z.-X. Du
Keyword(s):  
Thyroid Cancer ◽  
Tumor Necrosis Factor ◽  
Cancer Cells ◽  
Tumor Necrosis ◽  
Induced Apoptosis ◽  
Thyroid Cancer Cells ◽  
Necrosis Factor

scholarly journals Chrysin Sensitizes Human Lung Cancer Cells to Tumour Necrosis Factor Related Apoptosis-Inducing Ligand (TRAIL) Mediated Apoptosis

2019 ◽  
Vol 4 (2) ◽  
pp. 27-33
Author(s):  
Syed Hassan Mehdi ◽  
Md Zafaryab ◽  
Sana Nafees ◽  
Asad Khan ◽  
Irfan Ahmad ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Caspase 3 ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Induced Apoptosis ◽  
Necrosis Factor

Background: Lung cancer is the primary cause of cancer deaths worldwide. Thus, the requisite for more coherent methods to lung cancer therapy is needed. Purpose: Chrysin (5, 7-dihydroxyflavone) is a naturally occurring flavonoid having a wide range of pharmacological properties and is commonly found in fruits, vegetables, honey and propolis. In our study, we have hypothesized that chrysin would have anticancer activity on L132 lung cancer cell line.Methods: The cytotoxic effects were assessed by MTT and NRU assay. DAPI was used to evaluate the cell death. The pro- or anti-apoptotic proteins were detected by Western Blot assay, and, besides, mRNA expression was analysed with RT-PCR. In silico study of chrysin was performed to identify suitable inhibitors against the protein function. Results: Results indicated that chrysin enhanced the inhibitory effects of TRAIL (Tumour Necrosis Factor Related Apoptosis-Inducing Ligand) in comparison to TNF-α (tumour necrosis factor) on cell viability in L132 lung cancer cells and altered nuclear morphology of cells was observed in DAPI (4’,6-diamidino-2-phenylindole) staining after 48 hrs treatment. Treatment with chrysin enhances TRAIL-induced apoptosis by increasing the expression of apoptosis-related proteins including caspase-3, 8, 9 and Bax, whereas the expression of Bcl-2 was decreased. Chrysin was docked with caspase-3, 8, 9, Bax, and Bcl-2 proteins to identify suitable inhibitors against the protein function.Conclusion: We concluded that chrysin sensitizes lung cancer cells to TRAIL-induced apoptosis and may be considered for future studies as a promising therapeutic candidate for human lung cancer.

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