Related Experiment Video
Updated: May 26, 2026

Exploring the Pharmacological Action and Molecular Mechanism of Salidroside in Inhibiting MCF-7 Cell Proliferation and Migration
Published on: June 9, 2023
ERα signaling imparts chemotherapeutic selectivity to selenium nanoparticles in breast cancer
Kiritkumar K Vekariya1, Jasmine Kaur, Kulbhushan Tikoo
1Laboratory of Chromatin Biology, Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Nagar, Punjab, India.
Abstract:
The present study focuses on the synthesis of stable selenium nanoparticles (SeNPs) and the elucidation of their mechanism of action in preventing the growth of mammary tumors. Selenious acid and reduced glutathione in the presence of sodium alginate were used as precursors for synthesis of SeNPs. Cell viability and expression of apoptotic markers (pp38, Bax, and cytochrome c) were assessed in MCF-7 and MDA-MB-231 breast cancer cells treated with SeNPs. Reduction in tumor volume was measured in rats with dimethylbenz[a]anthracene-induced mammary tumors. Synthesized SeNPs ranged in size from 40 to 90 nm and were stable up to 3 months of storage. We report that SeNP-induced cell death and expression of pp38, Bax, and cytochrome c were significantly higher in estrogen receptor-α (ERα)-positive cells (MCF-7) but not in ERα-negative cells (MDA-MB-231). Interestingly, animals showing significant decrease in tumor volume (small tumors) had lower levels of ERα as compared with animals showing a nonsignificant decrease in tumor volume (large tumor). This is the first report in our knowledge suggesting that the anticancer activity of SeNPs correlates with the level of ERα in breast cancer cells both in vivo and in vitro.
From The Clinical Editor:
This study focuses on the synthesis of selenium nanoparticles (SeNPs) with the goal of preventing the growth of breast cancer cells, suggesting that the anticancer activity of SeNPs correlates with the level of ERα in breast cancer cells both in vivo and in vitro.
Insights
Stable selenium nanoparticles (SeNPs) show anticancer activity against breast cancer. Their effectiveness correlates with estrogen receptor-alpha (ERα) levels, being more potent in ERα-positive cells and reducing tumor volume in vivo.
Area of Science:
- Nanotechnology
- Biomedical Engineering
- Cancer Research
Background:
- Selenium nanoparticles (SeNPs) are synthesized for their potential anticancer properties.
- Previous research suggests SeNPs may inhibit cancer cell proliferation.
- The specific mechanism of SeNPs in breast cancer, particularly concerning estrogen receptor status, requires further elucidation.
Purpose of the Study:
- To synthesize stable selenium nanoparticles (SeNPs).
- To investigate the mechanism of action of SeNPs in preventing mammary tumor growth.
- To determine the correlation between SeNP anticancer activity and estrogen receptor-alpha (ERα) levels in breast cancer cells.
Main Methods:
- SeNPs synthesized using selenious acid, reduced glutathione, and sodium alginate.
- In vitro assessment of cell viability and apoptotic markers (pp38, Bax, cytochrome c) in MCF-7 and MDA-MB-231 cells.
- In vivo evaluation of tumor volume reduction in a rat model of chemically induced mammary tumors.
Main Results:
- Synthesized SeNPs were stable (40-90 nm, stable for 3 months).
- SeNP treatment significantly increased apoptosis markers and reduced viability in ERα-positive MCF-7 cells, but not in ERα-negative MDA-MB-231 cells.
- In vivo studies showed a significant decrease in tumor volume correlated with lower ERα levels.
Conclusions:
- SeNP anticancer activity is linked to ERα expression in breast cancer.
- SeNPs demonstrate potential as a therapeutic agent for ERα-positive breast cancers.
- This study provides novel insights into the in vivo and in vitro correlation between SeNP efficacy and ERα levels.
Related Concept Videos
Mitogens and the Cell Cycle
Targeted Cancer Therapies
There are several types of targeted therapies against specific...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
