Related Experiment Video

Updated: Jan 11, 2026

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter
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Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter

Published on: March 27, 2020

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Transcriptional enhanced associate domain factor 1 regulates cortactin-binding protein 2 N-terminal-like to control

Qian Ma1,2, Liyong Zhang1, Shan Jiang1

  • 1Department of Thyroid Surgery, Fujian Medical University Union Hospital, Fuzhou, China.

Cytojournal
|November 11, 2025
PubMed
Abstract

Insights

Transcriptional enhanced associate domain factor 1 (TEAD1) compensates for cortactin-binding protein 2 N-terminal-like (CTTNBP2NL) deficiency in papillary thyroid carcinoma (PTC). TEAD1 promotes PTC cell survival and growth, indicating its potential as a therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Papillary thyroid carcinoma (PTC) molecular mechanisms require elucidation for drug target identification.
  • Transcriptional enhanced associate domain factor 1 (TEAD1) and cortactin-binding protein 2 N-terminal-like (CTTNBP2NL) roles in PTC are not fully understood.

Purpose of the Study:

  • To investigate the molecular interactions between TEAD1 and CTTNBP2NL in PTC cells.
  • To assess the impact of these interactions on PTC cell proliferation, apoptosis, and clonogenicity.

Main Methods:

  • Differential gene expression analysis of TEAD1 and CTTNBP2NL in PTC tissues.
  • Correlation analysis of gene expression with patient survival.
  • In vitro experiments using TPC1 cells with manipulated TEAD1 and CTTNBP2NL levels.
  • Molecular biochemistry, cell proliferation, and colony formation assays.

Main Results:

  • TEAD1 and CTTNBP2NL expression levels significantly correlated with overall patient survival in PTC.
  • TEAD1 overexpression mitigated CTTNBP2NL downregulation effects, reducing proliferation and increasing apoptosis in TPC1 cells.
  • TEAD1 promoted cell proliferation and colony formation, while CTTNBP2NL silencing diminished cell growth.

Conclusions:

  • TEAD1 plays a compensatory role in PTC by alleviating CTTNBP2NL deficiency, promoting cell survival and growth.
  • TEAD1 represents a potential therapeutic target for papillary thyroid carcinoma.
Keywords:
ApoptosisCancerCortactin-binding proteinPapillary thyroid carcinomaProliferation

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