MEG3 as a transcriptional regulator of the DLK1-DOI3 region in human thyroid tumor cell lines

• Grant number: 25/11559-6
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: August 01, 2025
• End date: July 31, 2026
• Field of knowledge: Biological Sciences - Morphology - Cytology and Cell Biology
• Principal Investigator: Murilo Vieira Geraldo
• Grantee: Isabella Barbosa Cipriano da Silva
• Host Institution: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil

Abstract

Thyroid cancer cases increase in number over the years and, although most are treatable, variants such as anaplastic carcinoma are aggressive and have low survival rates. In this sense, recent studies by our group have shown the participation of different non-coding RNAs originating from the DLK1-DIO3 region in tumor progression, such as microRNAs and the long non-coding RNA MEG3. It is known that lncRNAs can act as local regulators of gene expression and, although MEG3 has emerged as a tumor suppressor in thyroid neoplasms, its function in the transcriptional control of the DLK1-DIO3 region is unknown. Thus, this project aims to build a gain-of-function model of MEG3 in thyroid tumor cell lines and evaluate the impact of its overexpression on the other genes in the DLK1-DIO3 region. The MEG3 gene will be cloned into a plasmid and transfected into papillary (TPC-1 and BCPAP) and anaplastic (KTC-2 and 8305C) carcinoma cell lines. After confirmation of MEG3 overexpression, total RNA will be extracted and the expression of genes in the region (DLK1, RTL1, MEG8, MEG9 and DIO3), as well as different miRNAs, will be evaluated in comparison with cell lines transfected with empty plasmid. The results contribute to the understanding of the mechanisms of transcriptional control of the region and the role of MEG3 in biological processes in this carcinoma.