Related Experiment Video

Updated: Mar 3, 2026

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

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

Published on: December 19, 2018

6.9K

ER-α36 Interactions With Cytosolic Molecular Network in Acquired Tamoxifen Resistance

Azin Teymourzadeh1, Sepideh Mansouri1, Leila Farahmand1

  • 1Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR, Tehran, Iran.

Clinical Breast Cancer
|April 24, 2017
PubMed

Insights

Estrogen receptor alpha-36 (ER-α36) promotes tamoxifen resistance in breast cancer by activating estrogen-independent pathways. Understanding ER-α36's role is crucial for overcoming treatment resistance in estrogen receptor-positive breast cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Endocrinology

Background:

  • Breast cancer is a leading cause of death in women, with most tumors being estrogen receptor (ER) positive.
  • Anti-estrogen therapies targeting ER are standard treatments, but resistance often develops.
  • ER-α36, a variant estrogen receptor, is implicated in acquired resistance to these therapies.

Purpose of the Study:

  • To review the molecular pathways through which ER-α36 contributes to tamoxifen resistance.
  • To elucidate how ER-α36 promotes estrogen-independent growth in breast cancer cells.
  • To highlight the complexity of resistance mechanisms involving ER-α36.

Main Methods:

  • Literature review of studies investigating ER-α36 and tamoxifen resistance.
  • Analysis of molecular interactions between ER-α36, ER-α66, and growth factor receptors.
  • Survey of signaling pathways affected by ER-α36 expression.

Main Results:

  • ER-α36 interacts with epidermal growth factor receptors and ER-α66.
  • ER-α36 promotes over-activation of estrogen-independent pathways.
  • ER-α36 suppresses estrogen-dependent pathways, maintaining tumor growth during tamoxifen treatment.

Conclusions:

  • ER-α36 plays a significant role in the development of tamoxifen resistance in breast cancer.
  • ER-α36 facilitates a switch from estrogen-dependent to estrogen-independent growth.
  • Targeting ER-α36 may offer new strategies to overcome anti-estrogen therapy resistance.
Keywords:
Breast cancerCytosolic growth cascadesER-α36Molecular networkTamoxifen resistance

More Related Videos

Systems Biology of Metabolic Regulation by Estrogen Receptor Signaling in Breast Cancer10:36

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

Published on: March 17, 2016

11.0K
Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

19.2K

Related Concept Videos

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
56
Transducer Mechanism: Nuclear Receptors01:31

Transducer Mechanism: Nuclear Receptors

Nuclear receptors, or NRs, are unique transcription factors that regulate gene transcription and affect the cellular pathways involved in reproduction, development, or metabolism. Their ability to be stimulated by small lipophilic ligands and control vital cellular processes makes them ideal drug targets. Nearly 10-15% of currently prescribed drugs target these receptors.
About 48 different soluble family members of nuclear receptors are identified that can be divided into two main classes:
4.0K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
8.2K
Transducer Mechanism: Enzyme-Linked Receptors01:27

Transducer Mechanism: Enzyme-Linked Receptors

Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
Major types that are helpful drug targets include:
4.6K
Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu01:29

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
69
Target Cell Response to Hormones01:22

Target Cell Response to Hormones

Hormones intricately bind to receptors on the surface or within target cells, initiating a cascade of cellular responses.
Notably, the cellular response can be regulated by altering the number of receptors expressed in the cell. For example, prolonged exposure to elevated hormone levels results in a gradual decline or down-regulation in the number of receptors for that specific hormone on the cell surface. Conversely, in response to low hormone levels, cells may use up-regulation, producing an...
6.0K