Related Experiment Video

Updated: Jan 31, 2026

Profiling of Estrogen-regulated MicroRNAs in Breast Cancer Cells
16:24

Profiling of Estrogen-regulated MicroRNAs in Breast Cancer Cells

Published on: February 21, 2014

20.7K

Raloxifene nano-micelles effect on triple-negative breast cancer is mediated through estrogen receptor-β and

Khaled Greish1,2, Hayley Nehoff3, Fatemah Bahman1

  • 1a Department of Molecular Medicine, and Nanomedicine Unit , College of Medicine and Medical Sciences, Princess Al-Jawhara Center for Molecular Medicine and Inherited Disorders, Arabian Gulf University , Manama , Kingdom of Bahrain.

Journal of Drug Targeting
|January 8, 2019
PubMed

Insights

Nanoformulated raloxifene, encapsulated in styrene-maleic acid (SMA) micelles, shows enhanced effectiveness against triple-negative breast cancer (TNBC). This novel approach improves drug delivery and reduces tumor growth, offering new hope for TNBC management.

Area of Science:

  • Oncology
  • Nanomedicine
  • Pharmacology

Background:

  • Triple-negative breast cancer (TNBC) is an aggressive subtype lacking targeted therapies due to its heterogeneity.
  • Selective estrogen receptor modulators like raloxifene show potential but have low in vivo bioavailability.
  • Raloxifene's efficacy may extend beyond estrogen receptor-alpha, independent of its known mechanisms.

Purpose of the Study:

  • To improve the pharmacokinetic profile and therapeutic efficacy of raloxifene for TNBC treatment.
  • To investigate the anti-cancer effects of raloxifene encapsulated in styrene-maleic acid (SMA) micelles.
  • To explore the role of estrogen receptor-beta in the anti-tumor activity of SMA-raloxifene.

Main Methods:

  • Encapsulation of raloxifene into styrene-maleic acid (SMA) micelles.
  • In vitro cytotoxicity assays comparing micellar and free raloxifene.
  • Assessment of cellular uptake and effects on critical signaling pathways.
  • In vivo studies evaluating the anti-tumor efficacy of SMA-raloxifene in TNBC models.

Main Results:

  • Micellar raloxifene exhibited significantly higher cytotoxicity and cellular uptake compared to the free drug.
  • SMA-raloxifene demonstrated superior inhibition of TNBC tumor growth in vivo.
  • The therapeutic effect of SMA-raloxifene was partially mediated through estrogen receptor-beta.

Conclusions:

  • Styrene-maleic acid (SMA) micelle encapsulation enhances raloxifene's pharmacokinetic properties and anti-cancer activity in TNBC.
  • This nanoformulation represents a promising strategy for improving the management of triple-negative breast cancer.
  • Further research into estrogen receptor-beta's role could refine TNBC therapeutic approaches.
Keywords:
EGFRSERMTriple-negative breast cancermicellenanomedicineoestrogen receptor-βraloxifene

More Related Videos

Studying the Stoichiometry of Epidermal Growth Factor Receptor in Intact Cells using Correlative Microscopy09:16

Studying the Stoichiometry of Epidermal Growth Factor Receptor in Intact Cells using Correlative Microscopy

Published on: September 11, 2015

8.7K
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

10.9K

Related Concept Videos

Receptor-mediated Endocytosis01:39

Receptor-mediated Endocytosis

Overview
110.9K
Receptor-mediated Endocytosis01:20

Receptor-mediated Endocytosis

Receptor-mediated endocytosis is when bulk amounts of specific molecules are imported into a cell after binding to cell surface receptors. The molecules bound to these receptors are taken into the cell through inward folding of the cell surface membrane, which is eventually pinched off into a vesicle within the cell. Structural proteins, such as clathrin, coat the budding vesicle.
Clathrin-Mediated Endocytosis of LDL
One well-characterized example of receptor-mediated endocytosis is the...
7.8K
Internal Receptors01:31

Internal Receptors

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.
74.6K
Adrenergic Receptors: β Subtype01:26

Adrenergic Receptors: β Subtype

β-adrenoceptors have varied sensitivities towards adrenaline, noradrenaline, and isoprenaline. The order of agonist potency is as follows:
Isoprenaline > Adrenaline > Noradrenaline
Neurotransmitter binding to these receptors causes activation of adenylyl cyclase resulting in increased concentrations of cAMP and modulation of calcium ion channels within the cell. They are further classified into β1, β2, and β3 subtypes.
β1-adrenoceptors: β1-adrenoceptors...
3.8K
Adrenergic Antagonists: ɑ and β-Receptor Blockers01:31

Adrenergic Antagonists: ɑ and β-Receptor Blockers

Third-generation β-blockers, such as labetalol and carvedilol, represent a significant advancement in managing cardiovascular conditions. Unlike conventional β-blockers, which can induce peripheral vasoconstriction, third-generation drugs block α1 adrenoceptors. This promotes vasodilation through several mechanisms, such as increased nitric oxide production, inhibition of calcium ion entry, opening of potassium ion channels, and antioxidant action. Labetalol, for instance, is...
1.2K
Enzyme-linked Receptors01:00

Enzyme-linked Receptors

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...
86.5K