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Related Experiment Video

Updated: Mar 31, 2026

Detecting the Ligand-binding Domain Dimerization Activity of Estrogen Receptor Alpha Using the Mammalian Two-Hybrid Assay

Detecting the Ligand-binding Domain Dimerization Activity of Estrogen Receptor Alpha Using the Mammalian Two-Hybrid Assay

Published on: December 19, 2018

Methyltransferase-like 17 physically and functionally interacts with estrogen receptors.

Peiyun Du¹, Bin Yuan¹, Jia Cao¹

¹Department of Medical Molecular Biology, Beijing Institute of Biotechnology, Beijing, People's Republic of China.

|October 22, 2015

Summary

Researchers discovered that methyltransferase-like 17 (METTL17) acts as a novel coactivator for estrogen receptors (ERs). METTL17 enhances ER transcriptional activity and breast cancer cell growth, suggesting a role in tumorigenesis.

Keywords:

estrogen receptor methyltransferase-like 17 transcriptional activity

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Systems Biology of Metabolic Regulation by Estrogen Receptor Signaling in Breast Cancer

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Published on: March 17, 2016

Area of Science:

Endocrinology
Molecular Biology
Cancer Research

Background:

Estrogen receptors (ERα and ERβ) regulate gene transcription and are crucial in physiological and pathological processes.
Coregulators are essential for modulating ER transcriptional activity, and novel ones are continuously sought.
The function of human methyltransferase-like 17 (METTL17) was previously unknown.

Purpose of the Study:

To investigate the function of METTL17 in relation to estrogen receptors.
To determine if METTL17 acts as a coregulator for ERα and ERβ.
To explore the potential role of METTL17 in breast cancer development.

Main Methods:

In vitro, yeast, and mammalian cell-based assays to assess physical interaction between METTL17 and ERs.
Analysis of ER activation function domains (AF1 and AF2) involved in METTL17 binding.
Gene knockdown and overexpression studies to evaluate METTL17's effect on ER transcriptional activity and target gene expression (PR, cathepsin D, pS2).
Assessment of METTL17's impact on breast cancer cell proliferation.

Main Results:

METTL17 physically interacts with both ERα and ERβ.
METTL17 functions as a coactivator for ERs, enhancing their transcriptional activity.
METTL17 knockdown inhibits ER activity and reduces the expression of ER target genes.
METTL17 overexpression boosts ER transcriptional activity.
METTL17 knockdown leads to decreased breast cancer cell growth.

Conclusions:

METTL17 is identified as a novel coactivator for estrogen receptors.
METTL17 plays a significant role in regulating ER transcriptional activity.
METTL17 may contribute to breast tumorigenesis and represents a potential therapeutic target.