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Related Concept Videos

Internal Receptors01:31

Internal Receptors

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Many cellular signals are hydrophilic and therefore cannot pass through the plasma membrane. However, small or hydrophobic signaling molecules can cross the hydrophobic core of the plasma membrane and bind to internal, or intracellular, receptors that reside within the cell. Many mammalian steroid hormones use this mechanism of cell signaling, as does nitric oxide (NO) gas.
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Enzyme-linked Receptors01:00

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Enzyme-linked receptors are proteins that act as both receptor and enzyme, activating multiple intracellular signals. This is a large group of receptors that include the receptor tyrosine kinase (RTK) family. Many growth factors and hormones bind to and activate the RTKs.
Neurotrophin (NT) receptors are a family of RTKs, including trkA, trkB, and trkC (tropomyosin-related kinase) receptors. TrkA is specific for nerve growth factor (NGF), neurotrophin-6, and neurotrophin-7. TrkB binds...
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G-protein Coupled Receptors01:21

G-protein Coupled Receptors

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G-protein coupled receptors are ligand binding receptors that indirectly affect changes in the cell. The actual receptor is a single polypeptide that transverses the cell membrane seven times creating intracellular and extracellular loops. The extracellular loops create a ligand specific pocket which binds to neurotransmitters or hormones. The intracellular loops holds onto the G-protein.
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Types of Receptors: Internal Receptors01:07

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Many cellular signals are hydrophilic and cannot pass through the plasma membrane. However, small or hydrophobic signaling molecules can cross the hydrophobic core of the plasma membrane and bind intracellular receptors that reside within the cell cytoplasm or nucleus. Many mammalian steroid hormones and nitric oxide (NO) gas use this cell signaling mechanism.
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Types of Receptors: Cell Surface Receptors01:28

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Cell-surface receptors, also known as transmembrane receptors, are cell surface, membrane-anchored (integral) proteins that bind to external ligand molecules. This type of receptor spans the plasma membrane and performs signal transduction, converting an extracellular signal into an intracellular signal. Ligands that interact with cell-surface receptors do not have to enter the cell that they affect. Cell-surface receptors are also called cell-specific proteins or markers because they are...
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Profiling of Estrogen-regulated MicroRNAs in Breast Cancer Cells
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Targeting mutant estrogen receptors.

Suzanne E Wardell1, John D Norris1, Donald P McDonnell1

  • 1Department of Pharmacology and Cancer Biology, Duke University School of Medicine, Durham, United States.

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|January 17, 2019
PubMed
Summary
This summary is machine-generated.

A hormone replacement therapy drug effectively targets estrogen receptors resistant to breast cancer treatments. This finding offers new hope for patients with advanced or treatment-resistant estrogen receptor-positive breast cancer.

Keywords:
SERM/SERDacquired drug resistancebazedoxifenebreast cancercancer biologyestrogen receptorhormone therapyhuman

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Area of Science:

  • Endocrinology
  • Oncology
  • Pharmacology

Background:

  • Estrogen receptors (ERs) are crucial in many breast cancers.
  • Resistance to endocrine therapies targeting ERs is a major clinical challenge.
  • Novel therapeutic strategies are needed for ER-positive breast cancer that has become resistant.

Purpose of the Study:

  • To investigate a hormone replacement therapy drug's efficacy against estrogen receptors resistant to standard breast cancer treatments.
  • To evaluate the drug's potential to overcome endocrine resistance in ER-positive breast cancer models.

Main Methods:

  • Utilized cell-based assays to assess drug activity on resistant ER variants.
  • Employed molecular biology techniques to analyze drug-target interactions.
  • Conducted preclinical studies to evaluate therapeutic potential.

Main Results:

  • The hormone replacement therapy drug demonstrated significant activity against estrogen receptors exhibiting resistance mechanisms.
  • The drug successfully inhibited proliferation in cancer cells with acquired endocrine resistance.
  • Specific molecular pathways modulated by the drug in resistant cells were identified.

Conclusions:

  • This hormone replacement therapy drug shows promise as a novel therapeutic agent for endocrine-resistant ER-positive breast cancer.
  • Targeting resistant estrogen receptors with this drug could offer a new treatment avenue.
  • Further clinical investigation is warranted to confirm its safety and efficacy in patients.