Related Experiment Video
Updated: Jun 8, 2025
Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
Published on: June 9, 2023
Blestriarene C exerts an inhibitory effect on triple-negative breast cancer through multiple signaling pathways
Junsha An1,2, Mingyu Han1, Hailin Tang3
1West China School of Pharmacy, Sichuan University, Chengdu, China.
Introduction:
Breast cancer is the most common cancer worldwide, the leading cause of cancer death in women, and the fifth leading cause of cancer death. Triple negative breast cancer (TNBC), with high metastasis and mortality rates, is the most challenging subtype in breast cancer treatment. There is an urgent need to develop anti-TNBC drugs with significant efficacy, low side effects and good availability. In early drug screening, blestriarene C was found to have inhibitory effects on TNBC cells. In this article, we further explore the mechanisms associated with blestriarene C for breast cancer.
Methods:
In this article, we take the approach of network pharmacology combined with in vivo and in vitro experiments. Network pharmacology analysis was used to predict the active components in Baiji, and to investigate the hub targets and related mechanisms of BC in TNBC treatment. The mechanism of anti-TNBC in vitro was evaluated by CCK-8 assay, cell apoptosis and cell cycle assays, wound healing assay, WB assay, and molecular docking analysis. The inhibition effect in vivo was test in subcutaneous tumor models established in mice.
Results:
Through network pharmacology analysis and experiments, we screened out BC as the main active ingredient, and found that BC could inhibit the Ras/ERK/c-Fos signaling pathway while downregulating the expression of HSP90AA1 and upregulating the expression of PTGS2, thereby promoting apoptosis, causing S-phase cycle arrest, and inhibiting the proliferation and migration of BT549 cells. The in vivo results illustrated that BC inhibited the growth of TNBC tumors and has a high safety profile. By integrating network pharmacology with in vitro and in vivo experiments, this study demonstrated that BC inhibited the proliferation and migration of TNBC cells by inhibiting the Ras/ERK/c-Fos signaling pathway, promoting apoptosis, and causing S-phase cycle arrest.
Discussion:
This study provides new evidence for the use of BC as a novel drug for TNBC treatment.
Insights
Blestriarene C (BC) effectively inhibits triple-negative breast cancer (TNBC) by targeting the Ras/ERK/c-Fos pathway, promoting apoptosis, and halting cell cycle progression. This natural compound shows promise as a safe and effective anti-TNBC therapeutic agent.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Triple-negative breast cancer (TNBC) presents significant treatment challenges due to high metastasis and mortality rates.
- There is a critical need for novel anti-TNBC drugs with improved efficacy and safety profiles.
- Blestriarene C (BC) was identified as a potential therapeutic agent with inhibitory effects on TNBC cells.
Purpose of the Study:
- To investigate the anti-TNBC mechanisms of blestriarene C (BC) using network pharmacology and experimental validation.
- To identify key molecular targets and pathways affected by BC in TNBC treatment.
- To evaluate the efficacy and safety of BC in both in vitro and in vivo TNBC models.
Main Methods:
- Network pharmacology was employed to predict active components and hub targets in TNBC.
- In vitro studies included CCK-8, apoptosis, cell cycle, wound healing, and Western blot assays.
- In vivo efficacy was assessed using a mouse subcutaneous tumor model, complemented by molecular docking analysis.
Main Results:
- Blestriarene C (BC) was identified as the primary active component, inhibiting the Ras/ERK/c-Fos signaling pathway.
- BC promoted apoptosis, induced S-phase cell cycle arrest, and inhibited proliferation and migration of BT549 TNBC cells.
- In vivo studies demonstrated BC's tumor growth inhibition in TNBC models with a favorable safety profile.
Conclusions:
- Blestriarene C (BC) effectively inhibits TNBC proliferation and migration by modulating the Ras/ERK/c-Fos pathway and inducing apoptosis and cell cycle arrest.
- The findings support BC as a potential novel therapeutic agent for triple-negative breast cancer.
- This study integrates network pharmacology with experimental data to elucidate BC's anti-TNBC mechanisms.
More Related Videos
08:48An In Vitro Dormancy Model of Estrogen-sensitive Breast Cancer in the Bone Marrow: A Tool for Molecular Mechanism Studies and Hypothesis Generation
Published on: June 30, 2015
06:54Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
Related Concept Videos
02:34Inhibition of Cdk Activity
01:19Interactions Between Signaling Pathways
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
02:57Targeted Cancer Therapies
There are several types of targeted therapies against...
02:38Mitogens and the Cell Cycle
01:17Intracellular Signaling Affects Focal Adhesions
Some...
01:16TGF - β Signaling Pathway