Synergistic activity of everolimus and 5‐aza‐2′‐deoxycytidine in medullary thyroid carcinoma cell lines

Mantovani, Giovanna; Dicitore, Alessandra; Pepe, Daniele; Gentilini, Davide; Grassi, Elisa; Borghi, Maria Orietta; Gelmini, Giulia; Cantone, Maria Celeste; Gaudenzi, Germano; Misso, Gabriella; Blasio, Anna Maria Di; Hofland, Leo J.; Caraglia, Michele; Persani, Luca

doi:10.1002/1878-0261.12070

Cited by 24 publications

(20 citation statements)

References 52 publications

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“…Among these, the neurotrophin signaling pathway was most directly involved in apoptosis, through NGFR and Bax gene overexpression. Increased expression of genes involved in the NGFR-MAPK10-TP53-Bax/Bcl2 pathway during incubation with AZA plus everolimus was validated by western blotting in MZ-CRC-1 cells [84].…”

Section: Sprouty1 (Spry1)mentioning

confidence: 90%

Research Progress of DNA Methylation in Thyroid Cancer

Zhu¹,

Xie²

2020

DNA Methylation Mechanism

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We have summarized increasing data from all kinds of experiment results of papers in recent years, which are associated with tumor suppressor genes, oncogenes, and thyroid-specific genes and attempt to elucidate the importance of epigenetic modifications and the mechanisms of aberrant DNA methylation in thyroid cancer in this review. The results showed that current articles have revealed the importance of epigenetic modifications and the different types of mechanisms in thyroid cancer. The mechanisms of DNA methylation related to thyroid cancer demonstrate that acquired epigenetic abnormalities together with genetic changes play an important role in alteration of gene expression patterns. Aberrant DNA methylation has been well known in the CpG regions. Among the genes identified, we have shown the status of DNA promoter methylation in papillary, follicular, medullary, and anaplastic thyroid cancer. It suggested that thyroid cancer subtypes present differential promoter methylation signatures, which will encourage potential thyroid cancer detection in its early stages, assessment of prognosis, and targeted cancer treatment.

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Section: Sprouty1 (Spry1)mentioning

confidence: 90%

Research Progress of DNA Methylation in Thyroid Cancer

Zhu¹,

Xie²

2020

DNA Methylation Mechanism

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“…For instance, a study found that the inhibition of CCDC69 was hypermethylated in ovarian cancer cells and might interfere with the effectiveness of combination therapy with platinum drugs, which means the combination of 5‐Aza‐dC and other anti‐cancer drugs may have better effect . To overcome drug resistance, some researchers explored a promising approach using 5‐Aza‐dC and the mTOR inhibitor everolimus in Medullary thyroid cancer cells, which showed a strong synergistic antiproliferative activity through the induction of apoptosis . Certainly, the studies of co‐treatment in renal cancer are not rare.…”

Section: Discussionmentioning

confidence: 99%

“…31 To overcome drug resistance, some researchers explored a promising approach using 5-Aza-dC and the mTOR inhibitor everolimus in Medullary thyroid cancer cells, which showed a strong synergistic antiproliferative activity through the induction of apoptosis. 32 Certainly, the studies of co-treatment in renal cancer are not rare.…”

Section: Discussionmentioning

confidence: 99%

PON1 hypermethylation is associated with progression of renal cell carcinoma

2019

J Cellular Molecular Medi

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In this study, our aim was to exploring the influences of DNA methylation of PON1 on cell proliferation, migration and apoptosis of renal cancer cells. The genome‐wide methylation array of renal cell carcinoma samples and adjacent tissues were obtained from the cancer genome atlas (TCGA) database. By analysing the DNA methylation and conducting the CpG islands array, methylation status expressed in renal tumour samples and normal renal tissue samples were detected. Methylation‐specific PCR (MS‐PCR) and qRT‐PCR were employed to detect the methylation level and mRNA expression of PON1. Wound‐healing assay, transwell assay and MTT assay were utilized to detecting the migration, invasion and proliferation abilities, respectively. The cell apoptosis was testified by Tunnel assay. In addition, the effect of PON1 on renal cancer cells was verified by experiments in vivo. The methylation status of different genes in renal cell carcinoma samples was obtained by CpG islands arrays and hypermethylated PON1 was selected for further study. PON1 was down‐regulated in renal cell carcinoma tissues detected by qRT‐PCR and Western blot. Both in vitro and vivo experiments indicated that the sunitinib‐resistant in renal cancer cells could be suppressed by treat with 5‐Aza‐dC or TSA, and the effect came out more obvious after 5‐Aza‐dC and TSA co‐treatment. In detail, the demethylation of PON1 inhibited the migration, invasion and proliferation of renal cancer cells and also arrested more cells in G0/G1 phase. The vivo experiment indicated that demethylated PON1 suppressed the growth of tumour. Hypermethylated PON1 promoted migration, invasion and proliferation of sunitinib‐resistance renal cancer cells and arrested more cells in G0/G1 phase.

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“…Compared with the results from the Venn diagram, all genes were included in RRA result. These iDEGs were predominantly enriched in the pathways 'PI3K-Akt signaling pathway', 'focal adhesion', 'ECM-receptor interaction' and the 'calcium signaling pathway' (24)(25)(26). A total of 7 hub genes were identified from the PPI network, which was composed of 493 iDEGs.…”

Section: Discussionmentioning

confidence: 99%

Integrated bioinformatics analysis to screen hub genes in the lymph node metastasis of thyroid cancer

Zhao

Shen

et al. 2019

Oncol Lett

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Thyroid cancer (TC) is one of the most common types of malignancy of the endocrine-system. At present, there is a lack of effective methods to predict neck lymph node metastasis (LNM) in TC. The present study compared the expression profiles from The Cancer Genome Atlas between N1M0 and N0M0 subgroups in each T1-4 stages TC in order to identify the four groups of TC LNM-associated differentially expressed genes (DEGs). Subsequently, DEGs were combined to obtain a total of 493 integrated DEGs by using the method of Robust Rank Aggregation. Furthermore, the underlying mechanisms of LNM were investigated. The results from Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses demonstrated that the identified DEGs may promote LNM via numerous pathways, including extracellular matrix-receptor interaction, PI3K-AKT signaling pathway and focal adhesion. Following construction of a protein-protein interaction network, the significance score for each gene was calculated and seven hub genes were screened, including interleukin 6, actinin α2, collagen type I α 1 chain, actin α1, calbindin 2, thrombospondin 1 and parathyroid hormone. These genes were predicted to serve crucial roles in TC with LNM. The results from the present study could therefore improve the understanding of LNM in TC. In addition, the seven DEGs identified may be considered as potential novel targets for the development of biomarkers that could be used in the diagnosis and therapy of TC.

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Synergistic activity of everolimus and 5‐aza‐2′‐deoxycytidine in medullary thyroid carcinoma cell lines

Cited by 24 publications

References 52 publications

Research Progress of DNA Methylation in Thyroid Cancer

Research Progress of DNA Methylation in Thyroid Cancer

PON1 hypermethylation is associated with progression of renal cell carcinoma

Integrated bioinformatics analysis to screen hub genes in the lymph node metastasis of thyroid cancer

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