ArticleJournal of cellular and molecular medicine2015
The c-MYC-ABCB5 axis plays a pivotal role in 5-fluorouracil resistance in human colon cancer cells.
Article in Journal of cellular and molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 66 citations in OpenAlex.
- Trial
- CCT2 enhances c-Myc stabilization to drive tumor progression and chemoresistance in head and neck squamous cell carcinoma.Genes & diseases · 2026Article
- Chitosan/β-cyclodextrin nanocarriers enhance 5-fluorouracil efficacy against colorectal cancer via pH-responsive release and apoptosis modulation.Scientific reports · 2026Article
- Everolimus destabilizes thymidylate synthase via suppressing its O-GlcNAcylation and sensitizes HER2-negative breast cancer to fluorouracil.Cell death & disease · 2026Article
- ABCB5: A Key Regulator Linking Stem Cell Plasticity, Tumor Microenvironment, and Therapy Resistance in Cutaneous Melanoma.Cancers · 2026Review
- Single-cell sequencing reveals the functional heterogeneity of melanoma cells and their crosstalk with the tumor microenvironment.Frontiers in genetics · 2026Article
- Resistance mechanism to pembrolizumab inInternational cancer conference journal · 2025Article
- A RareJournal of clinical medicine · 2025Article
- CF10/LV overcomes acquired resistance to 5-FU/LV in colorectal cancer cells through downregulation of the c-Myc/ABCB5 axis.Cancer drug resistance (Alhambra, Calif.) · 2025Article
- Stepwise Stiffening/Softening of and Cell Recovery from Reversibly Formulated Hydrogel Interpenetrating Networks.Advanced materials (Deerfield Beach, Fla.) · 2024Article
- Anti-Leukemic Effects of Small Molecule Inhibitor of c-Myc (10058-F4) on Chronic Myeloid Leukemia Cells.Asian Pacific journal of cancer prevention : APJCP · 2024Article
- MGMT activated by Wnt pathway promotes cisplatin tolerance through inducing slow-cycling cells and nonhomologous end joining in colorectal cancer.Journal of pharmaceutical analysis · 2024Article
- Stepwise Stiffening/Softening of and Cell Recovery from Reversibly Formulated Hydrogel Double Networks.bioRxiv : the preprint server for biology · 2024Article
- Identification of two novel heterodimeric ABC transporters in melanoma: ABCB5β/B6 and ABCB5β/B9.The Journal of biological chemistry · 2024Article
- The feedback loop of EFTUD2/c-MYC impedes chemotherapeutic efficacy by enhancing EFTUD2 transcription and stabilizing c-MYC protein in colorectal cancer.Journal of experimental & clinical cancer research : CR · 2024Article
- The uniqueness of ABCB5 as a full transporter ABCB5FL and a half-transporter-like ABCB5β.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- Review
- Skin-Derived ABCB5International journal of molecular sciences · 2022Review
- MYC and therapy resistance in cancer: risks and opportunities.Molecular oncology · 2022Review
- Drug-Tolerant Persister Cells in Cancer Therapy Resistance.Cancer research · 2022Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
c-MYC overexpression is frequently observed in various cancers including colon cancer and regulates many biological activities such as aberrant cell proliferation, apoptosis, genomic instability, immortalization and drug resistance. However, the mechanism by which c-MYC confers drug resistance remains to be fully elucidated. In this study, we found that the c-MYC expression level in primary colorectal cancer tissues correlated with the recurrence rate following 5-fluorouracil (5-FU)-based adjuvant chemotherapy. Supporting this finding, overexpression of exogenous c-MYC increased the survival rate following 5-FU treatment in human colon cancer cells, and knockdown of endogenous c-MYC decreased it. Furthermore, c-MYC knockdown decreased the expression level of ABCB5, which is involved in 5-FU resistance. Using a chromatin immunoprecipitation assay, we found that c-MYC bound to the ABCB5 promoter region. c-MYC inhibitor (10058-F4) treatment inhibited c-MYC binding to the ABCB5 promoter, leading to a decrease in ABCB5 expression level. ABCB5 knockdown decreased the survival rate following 5-FU treatment as expected, and the ABCB5 expression level was increased in 5-FU-resistant human colon cancer cells. Finally, using a human colon cancer xenograft murine model, we found that the combined 5-FU and 10058-F4 treatment significantly decreased tumorigenicity in nude mice compared with 5-FU or 10058-F4 treatment alone. 10058-F4 treatment decreased the ABCB5 expression level in the presence or absence of 5-FU. In contrast, 5-FU treatment alone increased the ABCB5 expression level. Taken together, these results suggest that c-MYC confers resistance to 5-FU through regulating ABCB5 expression in human colon cancer cells.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.