ArticleCell communication and signaling : CCS2022
BMX, a specific HDAC8 inhibitor, with TMZ for advanced CRC therapy: a novel synergic effect to elicit p53-, β-catenin- and MGMT-dependent apoptotic cell death.
Article in Cell communication and signaling : CCS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 15 citations in OpenAlex.
- Harnessing Tolypothrix sp. A-8 for biogenic synthesis of silver oxide nanoparticles (AgONPs) for multifunctional biomedical applications.Discover nano · 2026Article
- Repurposing pitavastatin and atorvastatin to overcome chemoresistance of metastatic colorectal cancer under high glucose conditions.Cancer cell international · 2025Article
- The effects of two combined methods of P53 expression and preoperative serum CEA detection on the prognosis of colorectal cancer.Frontiers in oncology · 2025Article
- Inhibition of HDAC8 mitigates AKI by reducing DNA damage and promoting homologous recombination repair.Journal of cellular and molecular medicine · 2024Article
- [Curcumol reverses temozolomide resistance in glioma cells by regulating the UTX/MGMT axis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Anticancer potential of biologically synthesized silver nanoparticles using Lantana camara leaf extract.Progress in biomaterials · 2023Article
- Fundamental concepts of protein therapeutics and spacing in oncology: an updated comprehensive review.Medical oncology (Northwood, London, England) · 2023Review
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14 authors at 7 institutions in 1 country.
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Abstract
backgroundDespite advances in treatment, patients with refractory colorectal cancer (CRC) still have poor long-term survival, so there is a need for more effective therapeutic options.
methodsTo evaluate the HDAC8 inhibition efficacy as a CRC treatment, we examined the effects of various HDAC8 inhibitors (HDAC8i), including BMX (NBM-T-L-BMX-OS01) in combination with temozolomide (TMZ) or other standard CRC drugs on p53 mutated HT29 cells, as well as wild-type p53 HCT116 and RKO cells.
resultsWe showed that HDAC8i with TMZ cotreatment resulted in HT29 arrest in the S and G2/M phase, whereas HCT116 and RKO arrest in the G0/G1 phase was accompanied by high sub-G1. Subsequently, this combination approach upregulated p53-mediated MGMT inhibition, leading to apoptosis. Furthermore, we observed the cotreatment also enabled triggering of cell senescence and decreased expression of stem cell biomarkers. Mechanistically, we found down-expression levels of β-catenin, cyclin D1 and c-Myc via GSK3β/β-catenin signaling. Intriguingly, autophagy also contributes to cell death under the opposite status of β-catenin/p62 axis, suggesting that there exists a negative feedback regulation between Wnt/β-catenin and autophagy. Consistently, the Gene Set Enrichment Analysis (GSEA) indicated both apoptotic and autophagy biomarkers in HT29 and RKO were upregulated after treating with BMX.
conclusionsBMX may act as a HDAC8 eraser and in combination with reframed-TMZ generates a remarkable synergic effect, providing a novel therapeutic target for various CRCs. Video Abstract.
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