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Molecular Biology of the Thyroid Cancer and Thyroid Dysfunctions
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Molecular Biology of the Thyroid Cancer and Thyroid Dysfunctions

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 June 2024 | Viewed by 5214

Special Issue Editor

Dr. Vija Lavinia

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Guest Editor
IUCT Oncopole Claudius Regaud, CRCT Oncology Research Centre Toulouse, University Paul Sabatier Toulouse, 31400 Toulouse, France
Interests: endocrine oncology; theragnostics; molecular targeted radiotherapy; Lu-177 dotatate; Lu-177 PSMA; thyroid cancer; prostate cancer; neuroendocrine tumors

Special Issue Information

Dear Colleagues,

Thyroid cancer and thyroid dysfunctions represent up to 2% of human disorders and a third of endocrine disorders. The field of thyroid disorders in endocrinology is growing, extending to thyroid dysfunctions related to new targeted and therapy-related immune-checkpoint inhibitors. Although there have been no significant changes in the prevalence and incidence of thyroid cancer, nor in its overall survival rate, recent progress in basic science, clinical studies, and translational research on this disease has led to new perspectives and improved understanding of thyroid disorders and thyroid oncogenesis.

The main objective of this Special Issue is to present original research on the molecular biology of thyroid cancer and thyroid dysfunctions. We hope to highlight new data on molecular pathways and metabolic characteristics that might advance our understanding of thyroid cancer and thyroid dysfunction development, paving the way for the discovery of new diagnostic options or new targeted or combined therapies.

The topics of this Special Issue include, but are not limited to:

  • Key biological processes such as: the cell cycle, DNA repair, apoptosis, autophagy, angiogenesis, invasion and metastasis, and signaling pathways.
  • Molecular thyroid pathology.
  • The thyroid cancer microenvironment.
  • The metabolic pathways involved in thyroid cancer.
  • Cancer epidemiology and prevention.
  • Cancer biomarkers: screening, diagnosis, treatment response, and prognosis.
  • Cancer therapy: target discovery, drug design, resistance, targeted therapy, theranostics, and personalized medicine.
  • Translational cancer research.
  • High-throughput technologies: genomics, epigenomics, proteomics, metabolomics, microarray, next-generation sequencing, and other omics technologies for thyroid dysfunctions.
  • Genomic and proteomic databases and their applications.

Dr. Lavinia M. Vija
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • animal models
  • apoptosis
  • autophagy
  • cancer biomarker
  • cancer epidemiology
  • cancer prevention
  • cancer screening
  • cholesterol metabolism
  • clinical trial
  • DNA repair
  • epigenomics
  • genome instability
  • genomic database
  • genomics
  • invasion
  • metabolomics
  • metastasis
  • methylation
  • microarray
  • microRNA
  • molecular diagnostics
  • molecular tumor pathology
  • next-generation sequencing
  • noncoding RNA
  • omics
  • personalized medicine
  • prognosis
  • proteomics
  • radionuclide therapy
  • signaling pathway
  • SNP genotyping
  • targeted therapy
  • theranostics
  • thyroid cancer
  • hyperthyroidism
  • therapeutic targets
  • translational cancer research
  • treatment response
  • tumor microenvironment

Published Papers (5 papers)

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Research

15 pages, 3930 KiB  
Article
Identification of Germline FOXE1 and Somatic MAPK Pathway Gene Alterations in Patients with Malignant Struma Ovarii, Cleft Palate and Thyroid Cancer
by Carolina Pires, Ana Saramago, Margarida M. Moura, Jing Li, Sara Donato, Inês J. Marques, Hélio Belo, Ana C. Machado, Rafael Cabrera, Thomas G. P. Grünewald, Valeriano Leite and Branca M. Cavaco
Int. J. Mol. Sci. 2024, 25(4), 1966; https://doi.org/10.3390/ijms25041966 - 6 Feb 2024
Viewed by 1069
Abstract
Germline variants in the FOXE1 transcription factor have been associated with thyroid ectopy, cleft palate (CP) and thyroid cancer (TC). Here, we aimed to clarify the role of FOXE1 in Portuguese families (F1 and F2) with members diagnosed with malignant struma ovarii (MSO), [...] Read more.
Germline variants in the FOXE1 transcription factor have been associated with thyroid ectopy, cleft palate (CP) and thyroid cancer (TC). Here, we aimed to clarify the role of FOXE1 in Portuguese families (F1 and F2) with members diagnosed with malignant struma ovarii (MSO), an ovarian teratoma with ectopic malignant thyroid tissue, papillary TC (PTC) and CP. Two rare germline heterozygous variants in the FOXE1 promoter were identified: F1) c.-522G>C, in the proband (MSO) and her mother (asymptomatic); F2) c.9C>T, in the proband (PTC), her sister and her mother (CP). Functional studies using rat normal thyroid (PCCL3) and human PTC (TPC-1) cells revealed that c.9C>T decreased FOXE1 promoter transcriptional activity in both cell models, while c.-522G>C led to opposing activities in the two models, when compared to the wild type. Immunohistochemistry and RT-qPCR analyses of patients’ thyroid tumours revealed lower FOXE1 expression compared to adjacent normal and hyperplastic thyroid tissues. The patient with MSO also harboured a novel germline AXIN1 variant, presenting a loss of heterozygosity in its benign and malignant teratoma tissues and observable β-catenin cytoplasmic accumulation. The sequencing of the F1 (MSO) and F2 (PTC) probands’ tumours unveiled somatic BRAF and HRAS variants, respectively. Germline FOXE1 and AXIN1 variants might have a role in thyroid ectopy and cleft palate, which, together with MAPK pathway activation, may contribute to tumours’ malignant transformation. Full article
(This article belongs to the Special Issue Molecular Biology of the Thyroid Cancer and Thyroid Dysfunctions)
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14 pages, 4519 KiB  
Article
Delving into the Role of lncRNAs in Papillary Thyroid Cancer: Upregulation of LINC00887 Promotes Cell Proliferation, Growth and Invasion
by Cristina Tous, Carmen Muñoz-Redondo, Angela Gavilán, Nereida Bravo-Gil, Fátima Baco-Antón, Elena Navarro-González, Guillermo Antiñolo and Salud Borrego
Int. J. Mol. Sci. 2024, 25(3), 1587; https://doi.org/10.3390/ijms25031587 - 27 Jan 2024
Cited by 2 | Viewed by 818
Abstract
Papillary thyroid carcinoma (PTC) is the most common histological category of thyroid cancer. In recent years, there has been an increasing number of studies on lncRNAs in PTC. Long intergenic non-protein coding RNA 887 (LINC00887) is a critical oncogene in developing other cancers. [...] Read more.
Papillary thyroid carcinoma (PTC) is the most common histological category of thyroid cancer. In recent years, there has been an increasing number of studies on lncRNAs in PTC. Long intergenic non-protein coding RNA 887 (LINC00887) is a critical oncogene in developing other cancers. LINC00887 is upregulated in PTC samples but its role in PTC is currently unclear. This study aimed to investigate the impact the disruption of LINC00887 expression has on PTC progression. We performed a CRISPR/Cas9 strategy for the truncation of LINC00887 in BCPAP and TPC1 cell lines. Functional assays showed that LINC00887 knockdown in both TPC1 and BCPAP cells reduced cell proliferation, colony formation and migration, delayed the cell cycle, and increased apoptosis. These results strengthened the role of LINC00887 in cancer and showed for the first time that this lncRNA could be a potential oncogene in PTC, acting as a tumor promoter. Modulation of the immune system may be one of the etiopathogenic mechanisms of LINC00887 in PTC, as shown by the observed influence of this lncRNA on PD-L1 expression. In addition, the biological pathways of LINC00887 identified to date, such as EMT, the Wnt/β-catenin signaling pathway or the FRMD6-Hippo signaling pathway may also be relevant regulatory mechanisms operating in PTC. Full article
(This article belongs to the Special Issue Molecular Biology of the Thyroid Cancer and Thyroid Dysfunctions)
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20 pages, 9510 KiB  
Article
Investigating USP42 Mutation as Underlying Cause of Familial Non-Medullary Thyroid Carcinoma
by Elisabete Teixeira, Cláudia Fernandes, Maria Bungărdean, Arnaud Da Cruz Paula, Raquel T. Lima, Rui Batista, João Vinagre, Manuel Sobrinho-Simões, Valdemar Máximo and Paula Soares
Int. J. Mol. Sci. 2024, 25(3), 1522; https://doi.org/10.3390/ijms25031522 - 26 Jan 2024
Viewed by 1000
Abstract
In a family with Familial Non-Medullary Thyroid Carcinoma (FNMTC), our investigation using Whole-Exome Sequencing (WES) uncovered a novel germline USP42 mutation [p.(Gly486Arg)]. USP42 is known for regulating p53, cell cycle arrest, and apoptosis, and for being reported as overexpressed in breast [...] Read more.
In a family with Familial Non-Medullary Thyroid Carcinoma (FNMTC), our investigation using Whole-Exome Sequencing (WES) uncovered a novel germline USP42 mutation [p.(Gly486Arg)]. USP42 is known for regulating p53, cell cycle arrest, and apoptosis, and for being reported as overexpressed in breast and gastric cancer patients. Recently, a USP13 missense mutation was described in FNMTC, suggesting a potential involvement in thyroid cancer. Aiming to explore the USP42 mutation as an underlying cause of FNMTC, our team validated the mutation in blood and tissue samples from the family. Using immunohistochemistry, the expression of USP42, Caspase-3, and p53 was assessed. The USP42 gene was silenced in human thyroid Nthy-Ori 3-1 cells using siRNAs. Subsequently, expression, viability, and morphological assays were conducted. p53, Cyclin D1, p21, and p27 proteins were evaluated by Western blot. USP42 protein was confirmed in all family members and was found to be overexpressed in tumor samples, along with an increased expression of p53 and cleaved Caspase-3. siRNA-mediated USP42 downregulation in Nthy-Ori 3-1 cells resulted in reduced cell viability, morphological changes, and modifications in cell cycle-related proteins. Our results suggest a pivotal role of USP42 mutation in thyroid cell biology, and this finding indicates that USP42 may serve as a new putative target in FNMTC. Full article
(This article belongs to the Special Issue Molecular Biology of the Thyroid Cancer and Thyroid Dysfunctions)
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21 pages, 1920 KiB  
Article
Expression of RASSF1A, DIRAS3, and AKAP9 Genes in Thyroid Lesions: Implications for Differential Diagnosis and Prognosis of Thyroid Carcinomas
by Kamila Soboska, Michał Kusiński, Karol Pawelczyk, Monika Migdalska-Sęk, Ewa Brzeziańska-Lasota and Karolina H. Czarnecka-Chrebelska
Int. J. Mol. Sci. 2024, 25(1), 562; https://doi.org/10.3390/ijms25010562 - 1 Jan 2024
Viewed by 937
Abstract
Thyroid carcinoma is the primary endocrine malignancy worldwide. The preoperative examination of thyroid tissue lesion is often unclear. Approximately 25% of thyroid cancers cannot be diagnosed definitively without post-surgery histopathological examination. The assessment of diagnostic and differential markers of thyroid cancers is needed [...] Read more.
Thyroid carcinoma is the primary endocrine malignancy worldwide. The preoperative examination of thyroid tissue lesion is often unclear. Approximately 25% of thyroid cancers cannot be diagnosed definitively without post-surgery histopathological examination. The assessment of diagnostic and differential markers of thyroid cancers is needed to improve preoperative diagnosis and reduce unnecessary treatments. Here, we assessed the expression of RASSF1A, DIRAS3, and AKAP9 genes, and the presence of BRAF V600E point mutation in benign and malignant thyroid lesions in a Polish cohort (120 patients). We have also performed a comparative analysis of gene expression using data obtained from the Gene Expression Omnibus (GEO) database (307 samples). The expression of RASSF1A and DIRAS3 was decreased, whereas AKAP9’s was increased in pathologically changed thyroid compared with normal thyroid tissue, and significantly correlated with e.g., histopathological type of lesion papillary thyroid cancer (PTC) vs follicular thyroid cancer (FTC), patient’s age, tumour stage, or its encapsulation. The receiver operating characteristic (ROC) analysis for the more aggressive FTC subtype differential marker suggests value in estimating RASSF1A and AKAP9 expression, with their area under curve (AUC), specificity, and sensitivity at 0.743 (95% CI: 0.548–0.938), 82.2%, and 66.7%; for RASSF1A, and 0.848 (95% CI: 0.698–0.998), 54.8%, and 100%, for AKAP9. Our research gives new insight into the basis of the aggressiveness and progression of thyroid cancers, and provides information on potential differential markers that may improve preoperative diagnosis. Full article
(This article belongs to the Special Issue Molecular Biology of the Thyroid Cancer and Thyroid Dysfunctions)
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16 pages, 3155 KiB  
Article
The Use of Tissue-on-Chip Technology to Focus the Search for Extracellular Vesicle miRNA Biomarkers in Thyroid Disease
by Thomas Haigh, Hannah Beattie, Mark A. Wade, James England, Dmitriy Kuvshinov, Laszlo Karsai, John Greenman and Victoria Green
Int. J. Mol. Sci. 2024, 25(1), 71; https://doi.org/10.3390/ijms25010071 - 20 Dec 2023
Viewed by 860
Abstract
Small extracellular vesicles (sEVs) contain microRNAs (miRNAs) which have potential to act as disease-specific biomarkers. The current study uses an established method to maintain human thyroid tissue ex vivo on a tissue-on-chip device, allowing the collection, isolation and interrogation of the sEVs released [...] Read more.
Small extracellular vesicles (sEVs) contain microRNAs (miRNAs) which have potential to act as disease-specific biomarkers. The current study uses an established method to maintain human thyroid tissue ex vivo on a tissue-on-chip device, allowing the collection, isolation and interrogation of the sEVs released directly from thyroid tissue. sEVs were analysed for differences in miRNA levels released from benign thyroid tissue, Graves’ disease tissue and papillary thyroid cancer (PTC), using miRNA sequencing and quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) to identify potential biomarkers of disease. Thyroid biopsies from patients with benign tissue (n = 5), Graves’ disease (n = 5) and PTC (n = 5) were perfused with medium containing sEV-depleted serum for 6 days on the tissue-on-chip device. During incubation, the effluents were collected and ultracentrifuged to isolate sEVs; miRNA was extracted and sequenced (miRNASeq). Out of the 15 samples, 14 passed the quality control and miRNASeq analysis detected significantly higher expression of miR-375-3p, miR-7-5p, miR-382-5p and miR-127-3p in the sEVs isolated from Graves’ tissue compared to those from benign tissue (false discovery rate; FDR p < 0.05). Similarly, miR-375-3p and miR-7-5p were also detected at a higher level in the Graves’ tissue sEVs compared to the PTC tissue sEVs (FDR p < 0.05). No significant differences were observed between miRNA in sEVs from PTC vs. those from benign tissue. These results were supported by Quantitative Reverse Transcriptase Polymerase Chain Reaction (qRT-PCR). The novel findings demonstrate that the tissue-on-chip technology is a robust method for isolating sEVs directly from the tissue of interest, which has permitted the identification of four miRNAs, with which further investigation could be used as biomarkers or therapeutic targets within thyroid disease. Full article
(This article belongs to the Special Issue Molecular Biology of the Thyroid Cancer and Thyroid Dysfunctions)
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