Comprehensive Characterization of Differentially Expressed Genes in Thyroid Cancer

Wang, Jian; Chi, Shumei; Huang, Zhongke; Ye, Xiaojuan; Shi, Guohua; Chen, Dongfang; Lou, Cen

doi:10.2217/fon-2017-0168

Cited by 10 publications

(8 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…23 Target drugs on specific genes related to thyroid carcinoma, including BRAF and RET, contribute to improve the clinical outcome of affected people. 24 After active treatment of surgical resection combined radioactive iodine and thyroid hormone suppression therapy, thyroid carcinoma patients usually achieve a satisfied prognosis. 25 Previous studies have shown that RNA methylation accounts for over 60% of all RNA modifications, including m 6 A, m 1 A and m 5 C, etc.…”

Section: Discussionmentioning

confidence: 99%

<p>Progression of Thyroid Carcinoma Is Promoted by the m6A Methyltransferase METTL3 Through Regulating m6A Methylation on TCF1</p>

Wang¹,

Jiang²,

Zhang³

et al. 2020

OTT

View full text Add to dashboard Cite

Objective: This study aims to uncover the progression of thyroid carcinoma influenced by the m6A methyltransferase METTL3 through regulating m 6 A methylation on TCF1 mRNA and the activated Wnt pathway. Methods: Thyroid carcinoma tissues and paracancerous ones were collected for detecting levels of METTL3 and TCF1. Potential correlation between levels of METTL3 and TCF1 was analyzed by Pearson analysis. Survival of thyroid carcinoma patients influenced by METTL3 level was assessed by Kaplan-Meier method. Regulatory effect of METTL3 on migratory ability in TPC-1 cells was examined by wound healing assay. The interaction between METTL3 with TCF1 and IGF2BP2 was verified by RNA-Binding Protein Immunoprecipitation (RIP) assay. Meanwhile, the activity of the Wnt pathway was reflected by TOP/FOP-Flash. At last, rescue experiments were conducted to clarify the involvement of TCF1 in phenotype changes of thyroid carcinoma cells that were regulated by METTL3. Results: METTL3 and TCF1 were upregulated in thyroid carcinoma. Similarly, METTL3 was highly expressed in thyroid carcinoma cells as well. Kaplan-Meier method uncovered poor prognosis in thyroid carcinoma patients expressing a high level of METTL3. Silence of METTL3 inhibited migratory ability and Wnt activity in TPC-1 cells. RIP assay confirmed the interaction between TCF1 and METTL3 or IGF2BP2. Moreover, METTL3 positively regulated the enrichment abundance of TCF1 in anti-IGF2BP2. Rescue experiments demonstrated that TCF1 was responsible for METTL3-regulated thyroid carcinoma progression via the m 6 A methylation. Conclusion: Upregulated m6A methyltransferase METTL3 promotes the progression of thyroid carcinoma through m 6 A methylation on TCF1.

show abstract

Section: Discussionmentioning

confidence: 99%

<p>Progression of Thyroid Carcinoma Is Promoted by the m6A Methyltransferase METTL3 Through Regulating m6A Methylation on TCF1</p>

Wang¹,

Jiang²,

Zhang³

et al. 2020

OTT

View full text Add to dashboard Cite

show abstract

“…Increased proliferation and cyclin activity are also hallmarks of cancer cells (Chai et al, 2016a), thus we aimed to characterize the expression of genes that have previously been shown to be up-or downregulated in thyroid cancer (Agrawal et al, 2014;Chai et al, 2016b;Costa et al, 2015;Wang et al, 2017). Interestingly, 72% of genes described as upregulated in thyroid cancer were downregulated in early passage (passage 0-2) organoids compared with primary tissue-derived cells, while some of these genes displayed further downregulation in later passage (passage 3-4) organoids ( Figure 4A, Table S3).…”

Section: Lack Of Thyroid Tumor Markers In Thyroid Organoidsmentioning

confidence: 99%

Generation and Differentiation of Adult Tissue-Derived Human Thyroid Organoids

et al. 2021

View full text Add to dashboard Cite

Total thyroidectomy as part of thyroid cancer treatment results in hypothyroidism requiring lifelong daily thyroid hormone replacement. Unbalanced hormone levels result in persistent complaints such as fatigue, constipation, and weight increase. Therefore, we aimed to investigate a patient-derived thyroid organoid model with the potential to regenerate the thyroid gland. Murine and human thyroidderived cells were cultured as organoids capable of self-renewal and which expressed proliferation and putative stem cell and thyroid characteristics, without a change in the expression of thyroid tumor-related genes. These organoids formed thyroid-tissue-resembling structures in culture. (Xeno-)transplantation of 600,000 dispersed organoid cells underneath the kidney capsule of a hypothyroid mouse model resulted in the generation of hormone-producing thyroid-resembling follicles. This study provides evidence that thyroid-lineagespecific cells can form organoids that are able to self-renew and differentiate into functional thyroid tissue. Subsequent (xeno-)transplantation of these thyroid organoids demonstrates a proof of principle for functional miniature gland formation.

show abstract

“…An investigation of differentially expressed genes (DEGs) between tumour and normal tissues may also help identify significant biomarkers. J. Wang et al () used the gene expression of 57 paired thyroid cancer and noncancerous tissues from the The Cancer Genome Atlas (TCGA) database to find 1,061 DEGs, including 752 upregulated and 309 downregulated genes. In addition, based on four Gene Expression Omnibus (GEO) microarray datasets, 225 commonly changed DEGs (111 upregulated and 114 downregulated) were identified (Liang & Sun, ).…”

Section: Introductionmentioning

confidence: 99%

Identification of key genes and pathways of thyroid cancer by integrated bioinformatics analysis

Liu

Zhou

et al. 2019

Journal Cellular Physiology

View full text Add to dashboard Cite

Thyroid cancer is a common endocrine malignancy with a rapidly increasing incidence worldwide. Although its mortality is steady or declining because of earlier diagnoses, its survival rate varies because of different tumour types. Thus, the aim of this study was to identify key biomarkers and novel therapeutic targets in thyroid cancer. The expression profiles of GSE3467, GSE5364, GSE29265 and GSE53157 were downloaded from the Gene Expression Omnibus database, which included a total of 97 thyroid cancer and 48 normal samples. After screening significant differentially expressed genes (DEGs) in each data set, we used the robust rank aggregation method to identify 358 robust DEGs, including 135 upregulated and 224 downregulated genes, in four datasets. Gene Ontology and Kyoto Encyclopaedia of Genes and Genomes pathway enrichment analyses of DEGs were performed by DAVID and the KOBAS online database, respectively. The results showed that these DEGs were significantly enriched in various cancer-related functions and pathways. Then, the STRING database was used to construct the protein-protein interaction network, and modules analysis was performed. Finally, we filtered out five hub genes, including LPAR5, NMU, FN1, NPY1R, and CXCL12, from the whole network. Expression validation and survival analysis of these hub genes based on the The Cancer Genome Atlas database suggested the robustness of the above results. In conclusion, these results provided novel and reliable biomarkers for thyroid cancer, which will be useful for further clinical applications in thyroid cancer diagnosis, prognosis and targeted therapy. K E Y W O R D Sbioinformatics, differentially expressed genes, GEO, robust rank aggregation, thyroid cancer

show abstract

Comprehensive Characterization of Differentially Expressed Genes in Thyroid Cancer

Abstract: These results provide some novel findings on DEGs in thyroid cancer, which will be useful to guide further investigation and target therapy for this disease. [Formula: see text].

Cited by 10 publications

References 31 publications

<p>Progression of Thyroid Carcinoma Is Promoted by the m6A Methyltransferase METTL3 Through Regulating m6A Methylation on TCF1</p>

<p>Progression of Thyroid Carcinoma Is Promoted by the m6A Methyltransferase METTL3 Through Regulating m6A Methylation on TCF1</p>

Generation and Differentiation of Adult Tissue-Derived Human Thyroid Organoids

Identification of key genes and pathways of thyroid cancer by integrated bioinformatics analysis

Contact Info

Product

Resources

About