ArticleNucleic acids research2019
New substituted quinoxalines inhibit triple-negative breast cancer by specifically downregulating the c-MYC transcription.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 109 citations in OpenAlex.
- MYC in Oncogenesis and Therapeutic Implications.MedComm · 2026Review
- G-quadruplex stabilization via small molecules as a potential anti-cancer strategy.Cellular & molecular biology letters · 2026Review
- Revealing G4 Structures as Drug Targets: Exploring the Potential of Novel Therapeutic Agents.Research (Washington, D.C.) · 2026Review
- Targeting MYC: Multidimensional regulation and therapeutic strategies in oncology.Genes & diseases · 2025Review
- Immunotherapy resistance in triple-negative breast cancer: Molecular mechanisms, tumor microenvironment, and therapeutic implications.Frontiers in oncology · 2025Review
- Discovery of Palbociclib as a potent c-Myc G4 stabilizer for lung cancer treatment using molecular docking, molecular dynamics simulation, and in vitro activity evaluation.Molecular diversity · 2024Article
- Harnessing Light for G-Quadruplex Modulation: Dual Isomeric Effects of anThe journal of physical chemistry letters · 2024Article
- A Phenotypic Approach to the Discovery of Potent G-Quadruplex Targeted Drugs.Molecules (Basel, Switzerland) · 2024Review
- Design and Optimization of Sesamol Nanosuspensions to Potentiate the Anti-Tumor Activity of Epirubicin against Ehrlich Solid Carcinoma-Bearing Mice.Pharmaceutics · 2024Article
- Moschus ameliorates glutamate-induced cellular damage by regulating autophagy and apoptosis pathway.Scientific reports · 2023Article
- G-Quadruplexes in c-MYC Promoter as Targets for Cancer Therapy.Biomedicines · 2023Review
- Crosstalk between G-quadruplex and ROS.Cell death & disease · 2023Review
- Strategies to target the cancer driver MYC in tumor cells.Frontiers in oncology · 2023Review
- MYC function and regulation in physiological perspective.Frontiers in cell and developmental biology · 2023Review
- 10-Gingerol Enhances the Effect of Taxol in Triple-Negative Breast Cancer via Targeting ADRB2 Signaling.Drug design, development and therapy · 2023Article
- Review
- Crosstalk between Hypoxia and Extracellular Matrix in the Tumor Microenvironment in Breast Cancer.Genes · 2022Review
- Interaction between non-coding RNAs, mRNAs and G-quadruplexes.Cancer cell international · 2022Review
- Development of a Smart Fluorescent Probe Specifically Interacting with C-Myc I-Motif.International journal of molecular sciences · 2022Article
- Major Achievements in the Design of Quadruplex-Interactive Small Molecules.Pharmaceuticals (Basel, Switzerland) · 2022Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Conventional chemotherapy remains the primary treatment option for triple-negative breast cancer (TNBC). However, the current chemotherapeutic drugs have limited effects on TNBC, and often lead to serious side effects as well as drug resistance. Thus, more effective therapeutic options are sorely needed. As c-MYC oncogene is highly expressed during TNBC pathogenesis, inhibiting c-MYC expression would be an alternative anti-TNBC strategy. In this study, we designed and synthesized a serial of quinoxaline analogs that target c-MYC promoter G-quadruplex (G4), which is believed to be a repressor of c-MYC transcription. Among them, a difluoro-substituted quinoxaline QN-1 was identified as the most promising G4-stabilizing ligand with high selectivity to c-MYC G4 over other G4s, which is distinguished from many other reported ligands. Intracellular studies indicated that QN-1 induced cell cycle arrest and apoptosis, repressed metastasis and inhibited TNBC cell growth, primarily due to the downregulation of c-MYC transcription by a G4-dependent mechanism. Notably, inhibition by QN-1 was significantly greater for c-MYC than other G4-driven genes. Cancer cells with c-MYC overexpression were more sensitive to QN-1, relative to normal cells. Furthermore, QN-1 effectively suppressed tumor growth in a TNBC mouse model. Accordingly, this work provides an alternative strategy for treating TNBC.
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