ArticleBMC cancer2024
Development of a novel treatment based on PKMYT1 inhibition for cisplatin-resistant bladder cancer with miR-424-5p-dependent cyclin E1 amplification.
Article in BMC cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- E2F1-mediated PKMYT1 upregulation promotes prostate cancer progression by inhibiting the PPAR signaling pathway.Scientific reports · 2025Article
- Dauriporphine inhibited lung cancer cell viability, motility, and energy metabolism through the miR-424-5p/MAPK14 axis.Hereditas · 2025Article
- PKMYT1 kinase ameliorates cisplatin sensitivity in osteosarcoma.Signal transduction and targeted therapy · 2025Article
- Engineered exosomes: a promising design platform for overcoming cancer therapy resistance.Frontiers in cell and developmental biology · 2025Review
- Gene expression silencing therapy in tumors, focus on gastrointestinal and genitourinary tumors.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChemotherapy including cisplatin is recommended for the treatment of advanced bladder cancer, but its effectiveness is limited due to the acquisition of drug resistance. Although several mechanisms of cisplatin resistance have been reported, there are still many unknowns, and treatment of cisplatin-resistant bladder cancer remains difficult. Accordingly, in this study, we aimed to identify and characterize microRNAs involved in cisplatin resistance.
methodsSmall RNA sequencing analysis was performed to search for microRNAs related to cisplatin resistance. The identified microRNAs were then characterized using gain-of-function studies, sensitivity analysis, target gene analysis, and cellular assays.
resultsWe identified miR-424-5p as a candidate microRNA that was downregulated in cisplatin-resistant strains compared with parental strains. Notably, in gain-of-function studies, miR-424-5p suppressed the proliferative ability of cisplatin-resistant bladder cancer (CDDP-R BC). Furthermore, miR-424-5p restored sensitivity to cisplatin. RNA sequence analysis revealed seven candidate genes targeted by this microRNA. Among them, cyclin E1 (CCNE1) was chosen for subsequent analyses because its expression was upregulated in cisplatin-resistant cells compared with parental cells and because recent studies have shown that CCNE1 amplification is synthetic lethal with PKMYT1 kinase inhibition. Therefore, we performed functional analysis using the PKMYT1 inhibitor RP-6306 and demonstrated that RP-6306 inhibited cell growth through suppression of mitotic entry and restored cisplatin sensitivity in CDDP-R BC.
conclusionsOverall, our findings provided insights into the development of novel therapeutic strategies for CDDP-R BC.
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