ENDOCRINE TUMOURS: Advances in the molecular pathogenesis of thyroid cancer: lessons from the cancer genome

Riesco‐Eizaguirre, Garcilaso; Santisteban, Pilar

doi:10.1530/eje-16-0202

Cited by 55 publications

(42 citation statements)

References 70 publications

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“…2,3 The carcinogenesis and tumor progression of thyroid cancer result from varieties of factors, including variation of gene expression and changing activity in signaling pathways. 4,5 Dysregulation of miRNAs has been documented to be implicated in a number of cancers, 8,9 including thyroid cancer. 10 Therefore, the exploration on miRNAs in thyroid cancer is helpful for the identification of potential biological markers for thyroid cancer.…”

Section: Discussionmentioning

confidence: 99%

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miR‐4319 inhibited the development of thyroid cancer by modulating FUS‐stabilized SMURF1

Bian

2019

J of Cellular Biochemistry

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Thyroid cancer, a common type of endocrine system cancer, has witnessed rising incidence and deaths over the past few years. The role of microRNAs is being increasingly discovered in a variety of cancers, including thyroid cancer. miR‐4319 has been elucidated in several studies to exert an antitumor function in multiple cancers but has never been explored in thyroid cancer. Our study proposed to explore the function and modulatory mechanism of miR‐4319 in thyroid cancer. First, we confirmed the downregulation of miR‐4319 in thyroid cancer tissues and cells, and revealed the correlation of miR‐4319 expression and clinical features in thyroid cancer. Functional assays illustrated that miR‐4319 attenuated proliferation, migration, and epithelial‐to‐mesenchymal transition (EMT) in thyroid cancer. Mechanistically, we identified through the miRDB database and proved that miR‐4319 targeted SMAD specific E3 ubiquitin protein ligase 1 (SMURF1). Furthermore, we discovered that miR‐4319 competed with fused in sarcoma (FUS) to bind to SMURF1, inhibiting the stabilization of SMURF1 messenger RNA. Rescue assays suggested that miR‐4319 retarded proliferation, migration, and EMT through SMURF1. Collectively, the results of this study showed that miR‐4319 inhibited the development of thyroid cancer by modulating FUS‐stabilized SMURF1, indicating miR‐4319 as a potent biological target for thyroid cancer.

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Section: Discussionmentioning

confidence: 99%

“…1 Past decades have witnessed a rising death rate due to the occurrence of thyroid cancer. 4,5 Therefore, effective therapeutic biological targets are in imminent need to be identified in thyroid cancer. 4,5 Therefore, effective therapeutic biological targets are in imminent need to be identified in thyroid cancer.…”

Section: Introductionmentioning

confidence: 99%

miR‐4319 inhibited the development of thyroid cancer by modulating FUS‐stabilized SMURF1

Bian

2019

J of Cellular Biochemistry

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“…A recent pan-cancer analysis on whole exome sequencing revealed that the mutation frequency in PTC was one of the lowest (approximately 1 change/Mb across the entire exome) among solid tumors (Lawrence et al 2013) (Fig. 4), while the mutation frequency in ATC was at the opposite extreme and was closer to that in melanoma and lung cancer, exceeding 100 changes/Mb (Kunstman et al 2015, Riesco-Eizaguirre & Santisteban 2016. As mutations are largely caused by errors in DNA replication (Tomasetti et al 2017), some researchers propose that the cell division rate also participates in shaping the cancer DNA methylation landscape (Yang et al 2016b).…”

Section: Dna Methylation Changes In Thyroid Cancer: Drivers Of Diseasmentioning

confidence: 92%

DNA methylation in thyroid cancer

Zafón

Gil

Pérez-González

et al. 2019

Endocrine-Related Cancer

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In recent years, cancer genomics has provided new insights into genetic alterations and signaling pathways involved in thyroid cancer. However, the picture of the molecular landscape is not yet complete. DNA methylation, the most widely studied epigenetic mechanism, is altered in thyroid cancer. Recent technological advances have allowed the identification of novel differentially methylated regions, methylation signatures and potential biomarkers. However, despite recent progress in cataloging methylation alterations in thyroid cancer, many questions remain unanswered. The aim of this review is to comprehensively examine the current knowledge on DNA methylation in thyroid cancer and discuss its potential clinical applications. After providing a general overview of DNA methylation and its dysregulation in cancer, we carefully describe the aberrant methylation changes in thyroid cancer and relate them to methylation patterns, global hypomethylation and gene-specific alterations. We hope this review helps to accelerate the use of the diagnostic, prognostic and therapeutic potential of DNA methylation for the benefit of thyroid cancer patients.

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“…Page 2 of 14 Liu et al J Transl Med (2020) 18:170 cancer [2]. In recent years, researchers believe that the major carcinogenic event of PTC is the activation of mitogen-activated protein kinase (MAPK) [3]. However, the mechanisms underlying the pathogenesis of PTC have not yet been elucidated.…”

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confidence: 99%

Identification of hub genes in papillary thyroid carcinoma: robust rank aggregation and weighted gene co-expression network analysis

et al. 2020

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Background: Papillary thyroid carcinoma (PTC), which is the most common endocrine malignancy, has been steadily increasing worldwide in incidence over the years, while mechanisms underlying the pathogenesis and diagnostic for PTC are incomplete. The purpose of this study is to identify potential biomarkers for diagnosis of PTC, and provide new insights into pathogenesis of PTC.Methods: Based on weighted gene co-expression network analysis, Robust Rank Aggregation, functional annotation, GSEA and DNA methylation, were employed for investigating potential biomarkers for diagnosis of PTC.Results: Black and turquoise modules were identified in the gene co-expression network constructed by 1807 DEGs that from 6 eligible gene expression profiles of Gene Expression Omnibus database based on Robust Rank Aggregation and weighted gene co-expression network analysis. Hub genes were significantly down-regulated and the expression levels of the hub genes were different in different stages in hub gene verification. ROC curves indicated all hub genes had good diagnostic value for PTC (except for ABCA6 AUC = 89.5%, the 15 genes with AUC > 90%). Methylation analysis showed that hub gene verification ABCA6, ACACB, RMDN1 and TFPI were identified as differentially methylated genes, and the decreased expression level of these genes may relate to abnormal DNA methylation. Moreover, the expression levels of 8 top hub genes were correlated with tumor purity and tumor-infiltrating immune cells. These findings, including functional annotations and GSEA provide new insights into pathogenesis of PTC. Conclusions:The hub genes and methylation of hub genes may as potential biomarkers provide new insights for diagnosis of PTC, and all these findings may be the direction to study the mechanisms underlying of PTC in the future.

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ENDOCRINE TUMOURS: Advances in the molecular pathogenesis of thyroid cancer: lessons from the cancer genome

Cited by 55 publications

References 70 publications

miR‐4319 inhibited the development of thyroid cancer by modulating FUS‐stabilized SMURF1

miR‐4319 inhibited the development of thyroid cancer by modulating FUS‐stabilized SMURF1

DNA methylation in thyroid cancer

Identification of hub genes in papillary thyroid carcinoma: robust rank aggregation and weighted gene co-expression network analysis

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