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Related Experiment Video

Updated: Jun 28, 2026

Detecting the Ligand-binding Domain Dimerization Activity of Estrogen Receptor Alpha Using the Mammalian Two-Hybrid Assay
09:07

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Published on: December 19, 2018

MCM7 interacts with androgen receptor.

Yi-Kang Shi1, Yan P Yu, Ze-Hua Zhu

  • 1Department of Pathology, University of Pittsburgh, Pittsburgh, PA 15090, USA.

The American Journal of Pathology
|November 8, 2008
PubMed
Summary
This summary is machine-generated.

Metastatic prostate cancer involves MCM7, a DNA replication protein. MCM7 interacts with the androgen receptor (AR), influencing DNA synthesis and proliferation, potentially bypassing AR blockade therapy.

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • MCM7 is a key component of the DNA replication licensing complex, essential for DNA replication control in various organisms.
  • MCM7 amplification and overexpression are observed in metastatic prostate cancer.
  • The androgen receptor (AR) plays a crucial role in prostate cancer development and progression.

Purpose of the Study:

  • To investigate the interaction between MCM7 and the androgen receptor (AR) in the context of prostate cancer.
  • To elucidate the functional consequences of the MCM7-AR interaction on DNA replication, gene expression, and cell proliferation.
  • To explore the potential role of this interaction in therapeutic resistance in prostate cancer.

Main Methods:

  • In vitro and in vivo assays to confirm MCM7-AR interaction and identify binding motifs.
  • Androgen stimulation experiments (R1881) to assess the effects on MCM7 binding to DNA, DNA synthesis, and cell proliferation.
  • Assessment of AR gene transcription and repressor activity using AR mutants and MCM7 knockdown.

Main Results:

  • MCM7 and AR interact with high affinity, with identified binding motifs on both proteins.
  • AR stimulation differentially affects MCM7 function: high doses decrease DNA replication and proliferation, while low doses increase them.
  • The MCM7-AR interaction down-regulates MCM7 expression and is essential for AR's gene transcription and repressor activities.

Conclusions:

  • AR and MCM7 mutually facilitate each other's function through a novel interaction mechanism.
  • AR-independent activation of MCM7 may represent a mechanism for prostate cancers to evade AR-targeted therapies.
  • Targeting the MCM7-AR interaction could offer new therapeutic strategies for overcoming treatment resistance in prostate cancer.