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Updated: Jun 17, 2026
Polymalic Acid-based Nano Biopolymers for Targeting of Multiple Tumor Markers: An Opportunity for Personalized Medicine?
Published on: June 13, 2014
Network-based exploration of 4-(phenylsulfonyl)morpholine molecules for metastatic triple-negative breast cancer
Jung-Chen Su1, Chen-Ling Lee2, Fan-Wei Yang1
1Department of Pharmacy, College of Pharmaceutical Sciences, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Abstract:
Triple-negative breast cancer (TNBC) is an aggressive and heterogeneous subtype of breast cancer, with limited treatment options due to the absence of estrogen receptors, progesterone receptors, and human epidermal growth factor receptor 2 (HER2) expression. This characteristic renders TNBC resistant to hormone-based and HER2-targeted therapies, leaving cytotoxic chemotherapy as the predominant strategy and highlighting the urgency for novel interventions. In this study, we investigated the mechanism of action of GL24, a potent 4-(phenylsulfonyl)morpholine-based small molecule with selective tumor suppression effects on metastatic TNBC cells, while being ineffective against TNBC cells derived from the primary tumor site, using gene co-expression analysis. By considering the distinct phenotypic responses induced by GL24, we tailored our co-expression analysis approach, selecting gene pairs that exhibited differential co-expression in effective cells while excluding gene pairs that also showed differential patterns in non-effective cells. Constructing a co-expression network from these differential pairs, followed by enrichment analysis and functional annotation, revealed specific gene interactions and molecular pathways associated with GL24-mediated TNBC inhibition. These insights supported the previously established findings that showed convergence on apoptosis based on differentially expressed genes, while also providing complementary information by highlighting pathways involved in metabolic alterations, proliferation, and migration or invasion. This expanded understanding advances the knowledge of the mechanisms of GL24 in combating TNBC.
Insights
A novel compound, GL24, shows selective tumor suppression in metastatic triple-negative breast cancer (TNBC) by targeting specific molecular pathways. This research uncovers new therapeutic strategies for aggressive TNBC by understanding GL24
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Triple-negative breast cancer (TNBC) is an aggressive subtype lacking standard therapeutic targets.
- Limited treatment options for TNBC necessitate the development of novel interventions.
- Existing therapies for TNBC primarily rely on cytotoxic chemotherapy.
Purpose of the Study:
- To investigate the mechanism of action of GL24, a small molecule with selective anti-TNBC effects.
- To identify molecular pathways modulated by GL24 in metastatic TNBC cells.
- To elucidate the differential effects of GL24 on metastatic versus primary TNBC cells.
Main Methods:
- Gene co-expression analysis tailored to differential cellular responses to GL24.
- Construction of a gene co-expression network from differentially co-expressed gene pairs.
- Enrichment analysis and functional annotation of the co-expression network.
Main Results:
- GL24 selectively suppresses metastatic TNBC cells, with no effect on primary tumor cells.
- Co-expression network analysis revealed pathways involved in apoptosis, metabolic alterations, proliferation, and migration/invasion.
- Findings support and expand upon previous knowledge of GL24's anti-cancer mechanisms.
Conclusions:
- GL24 demonstrates selective efficacy against metastatic TNBC, offering a potential targeted therapy.
- The study elucidates novel molecular pathways targeted by GL24, including metabolism and cell migration.
- Understanding GL24's mechanism advances therapeutic strategies for aggressive triple-negative breast cancer.
