DNA Methylation Gene Expression Genes, Tumor Suppressor NOL4 Thyroid Cancer, Papillary

Journal

International journal of endocrinology and metabolism
ISSN: 1726-913X
Titre abrégé: Int J Endocrinol Metab
Pays: Netherlands
ID NLM: 101235597

Informations de publication

Date de publication:
Oct 2020
Historique:
received: 15 08 2020
revised: 08 09 2020
accepted: 19 09 2020
entrez: 22 2 2021
pubmed: 23 2 2021
medline: 23 2 2021
Statut: epublish

Résumé

Thyroid cancer is the fourth most common cancer in the world. Papillary thyroid carcinoma (PTC) accounts for 80% of all types of thyroid neoplasm. Epigenetic alterations such as DNA methylation are known as the main cause of different types of cancers through inactivation of tumor suppressor genes. In the present study, the expression and methylation of suggested gene namely nucleolar protein 4 ( Forty-one patients with PTC and 38 patients affected by MNG were recruited. Thyroid tissues were obtained during thyroidectomy. RNA and DNA were extracted from thyroid tissues. Quantitative RT-PCR assay was performed for determining the mRNA level of Methylation assessment of 81 CpG islands in the promoter region of These data suggested an aberrant promoter hyper-methylation of

Sections du résumé

BACKGROUND BACKGROUND
Thyroid cancer is the fourth most common cancer in the world. Papillary thyroid carcinoma (PTC) accounts for 80% of all types of thyroid neoplasm. Epigenetic alterations such as DNA methylation are known as the main cause of different types of cancers through inactivation of tumor suppressor genes.
OBJECTIVES OBJECTIVE
In the present study, the expression and methylation of suggested gene namely nucleolar protein 4 (
METHODS METHODS
Forty-one patients with PTC and 38 patients affected by MNG were recruited. Thyroid tissues were obtained during thyroidectomy. RNA and DNA were extracted from thyroid tissues. Quantitative RT-PCR assay was performed for determining the mRNA level of
RESULTS RESULTS
Methylation assessment of 81 CpG islands in the promoter region of
CONCLUSIONS CONCLUSIONS
These data suggested an aberrant promoter hyper-methylation of

Identifiants

pubmed: 33613681
doi: 10.5812/ijem.108510
pmc: PMC7887463
doi:

Types de publication

Journal Article

Langues

eng

Pagination

e108510

Informations de copyright

Copyright © 2020, International Journal of Endocrinology and Metabolism.

Déclaration de conflit d'intérêts

Conflict of Interests: The authors declare no competing interests.

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Auteurs

Sara Sheikholeslami (S)

Cellular and Molecular Endocrine Research Center, Research Institute for Endocrine Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Fereidoun Azizi (F)

Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Asghar Ghasemi (A)

Endocrine Physiology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Abbas Alibakhshi (A)

Department of General Surgery, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran.

Hossein Parsa (H)

Department of Surgery, Velayat Hospital, Qazvin University of Medical Sciences, Qazvin, Iran.

Seyed Mohammad Tavangar (SM)

Department of Pathology, Dr. Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran.

Setareh Shivaee (S)

Cellular and Molecular Endocrine Research Center, Research Institute for Endocrine Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Marjan Zarif Yeganeh (M)

Cellular and Molecular Endocrine Research Center, Research Institute for Endocrine Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Mehdi Hedayati (M)

Cellular and Molecular Endocrine Research Center, Research Institute for Endocrine Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Ladan Teimoori-Toolabi (L)

Molecular Medicine Department, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran.

Classifications MeSH