The Role of the NIS (SLC5A5) Gene in Papillary Thyroid Cancer: A Systematic Review

Morais, Rafael Martins de; Sobrinho, Alaor Barra; Silva, Calliandra Maria de Souza; Oliveira, Jamila Reis de; Silva, Izabel Cristina Rodrigues da; Nóbrega, Otávio de Tolêdo

doi:10.1155/2018/9128754

Cited by 25 publications

(23 citation statements)

References 44 publications

(55 reference statements)

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“…Moreover, thyroid differentiation specific genes, as thyroid transcription factor-1 ( TTF1 ) and sodium-iodide symporter ( NIS) , are also hypermethylated particularly in undifferentiated tumors ( 50 ). High expression levels of DNMT1 have been associated with silencing of NIS ( 51 ). The role of KISS1/KISS1R signaling is controversial in various types of cancers, as it has been associated with both roles in metastatic promotion and suppression ( 52 – 54 ).…”

Section: Epigenetic Alterations Sustaining Tcscs Origin and Maintenaimentioning

confidence: 99%

Cancer Stem Cells in Thyroid Tumors: From the Origin to Metastasis

et al. 2020

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Thyroid tumors are extremely heterogeneous varying from almost benign tumors with good prognosis as papillary or follicular tumors, to the undifferentiated ones with severe prognosis. Recently, several models of thyroid carcinogenesis have been described, mostly hypothesizing a major role of the thyroid cancer stem cell (TCSC) population in both cancer initiation and metastasis formation. However, the cellular origin of TCSC is still incompletely understood. Here, we review the principal epigenetic mechanisms relevant to TCSC origin and maintenance in both well-differentiated and anaplastic thyroid tumors. Specifically, we describe the alterations in DNA methylation, histone modifiers, and microRNAs (miRNAs) involved in TCSC survival, focusing on the potential of targeting aberrant epigenetic modifications for developing novel therapeutic approaches. Moreover, we discuss the bidirectional relationship between TCSCs and immune cells. The cells of innate and adaptive response can promote the TCSC-driven tumorigenesis, and conversely, TCSCs may favor the expansion of immune cells with protumorigenic functions. Finally, we evaluate the role of the tumor microenvironment and the complex cross-talk of chemokines, hormones, and cytokines in regulating thyroid tumor initiation, progression, and therapy refractoriness. The re-education of the stromal cells can be an effective strategy to fight thyroid cancer. Dissecting the genetic and epigenetic landscape of TCSCs and their interactions with tumor microenvironment cells is urgently needed to select more appropriate treatment and improve the outcome of patients affected by advanced differentiated and undifferentiated thyroid cancers.

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Section: Epigenetic Alterations Sustaining Tcscs Origin and Maintenaimentioning

confidence: 99%

Cancer Stem Cells in Thyroid Tumors: From the Origin to Metastasis

et al. 2020

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“…More recently, accumulating literature has emerged providing evidence emphasizing the crucial role of DPP4 in the immune system, especially in the release of T cells . The solute carrier family 5 member 5 (SLC5A5, National Inpatient Sample) gene, located on chromosome 19 (19p13.11), encodes a highly specialized 80–90 kDa transmembrane glycoprotein that helps to regulate the active transport of iodide from the blood into the follicular cells . Guerrieri et al .…”

Section: Discussionmentioning

confidence: 99%

“…29 The solute carrier family 5 member 5 (SLC5A5, National Inpatient Sample) gene, located on chromosome 19 (19p13.11), encodes a highly specialized 80-90 kDa transmembrane glycoprotein that helps to regulate the active transport of iodide from the blood into the follicular cells. 30 Guerrieri et al 31 concluded that SLC5A5 is a direct target gene of the p53 signaling pathway and suggested that the DNA-damaging agents-mediated SLC5A5 could hypothetically potentiate its upregulation in vivo. Solute-linked carrier has been linked to disease resistance and susceptibility in animals, with research proposing its potential as an essential mechanism in the mediation against intracellular infection.…”

Section: (A) (B)mentioning

confidence: 99%

Identification of Susceptibility Genes to Allergic Rhinitis by Gene Expression Data Sets

Xue

Yang

Zhao

et al. 2019

Clinical Translational Sci

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As an extremely prevalent disease worldwide, allergic rhinitis (AR) is a condition characterized by chronic inflammation of the nasal mucosa. To identify the finer molecular mechanisms associated with the AR susceptibility genes, differentially expressed genes (DEGs) in AR were investigated. The DEG expression and clinical data of the GSE19187 data set were used for weighted gene co‐expression network analysis (WGCNA). After the modules related to AR had been screened, the genes in the module were extracted for Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, whereby the genes enriched in the KEGG pathway were regarded as the pathway‐genes. The DEGs in patients with AR were subsequently screened out from GSE19187, and the sensitive genes were identified in GSE18574 in connection with the allergen challenge. Two kinds of genes were compared with the pathway‐genes in order to screen the AR susceptibility genes. Receiver operating characteristic (ROC) curve was plotted to evaluate the capability of the susceptibility genes to distinguish the AR state. Based on the WGCNA in the GSE19187 data set, 10 co‐expression network modules were identified. The correlation analyses revealed that the yellow module was positively correlated with the disease state of AR. A total of 89 genes were found to be involved in the enrichment of the yellow module pathway. Four genes (CST1, SH2D1B, DPP4, and SLC5A5) were upregulated in AR and sensitive to allergen challenge, whose potentials were further confirmed by ROC curve. Taken together, CST1, SH2D1B, DPP4, and SLC5A5 are susceptibility genes to AR.

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“…Accordingly, the decreased NIS expression and/or impairment in NIS plasma membrane trafficking (De la Vieja & Santisteban 2018) are well demonstrated factors showing poor prognosis in thyroid cancer. However, the relationship between NIS and thyroid cancer is complex and not well understood (de Morais et al 2018). Mutations in the NIS gene do not appear to be a major cause for reduced NIS expression/ function in thyroid cancer (Russo et al 2001).…”

Section: Focal Dna Methylation Alterations In Thyroid Cancer: Gene-spmentioning

confidence: 99%

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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The Role of the NIS (SLC5A5) Gene in Papillary Thyroid Cancer: A Systematic Review

Cited by 25 publications

References 44 publications

Cancer Stem Cells in Thyroid Tumors: From the Origin to Metastasis

Cancer Stem Cells in Thyroid Tumors: From the Origin to Metastasis

Identification of Susceptibility Genes to Allergic Rhinitis by Gene Expression Data Sets

DNA methylation in thyroid cancer

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