ArticleJournal of cellular and molecular medicine2025
Bayesian-optimized deep learning for identifying essential genes of mitophagy and fostering therapies to combat drug resistance in human cancers.
Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Exercise as a Programmable Regulator of Mitophagy Sensitivity in Aging Muscle and Age-Related Disease.IUBMB life · 2026Review
- Enhanced MIF/CD74 axis activity shapes B cell functioning following traumatic spinal cord injury.Journal of neuroinflammation · 2026Article
- GeneCytNet: an interpretable deep learning framework for rheumatoid arthritis classification andFrontiers in immunology · 2026Article
- Leveraging artificial intelligence in antibody-drug conjugate development: from target identification to clinical translation in oncology.NPJ precision oncology · 2025Review
- Gradient responsive regularization: a deep learning framework for codon frequency based classification of evolutionarily conserved genes.BMC genomic data · 2025Article
- Bayesian-optimized deep learning for identifying essential genes of mitophagy and fostering therapies to combat drug resistance in human cancers.Journal of cellular and molecular medicine · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Dysregulated mitophagy is essential for mitochondrial quality control within human cancers. However, identifying hub genes regulating mitophagy and developing mitophagy-based treatments to combat drug resistance remains challenging. Herein, BayeDEM (Bayesian-optimized Deep learning for identifying Essential genes of Mitophagy) was proposed for such a task. After Bayesian optimization, BayeDEM demonstrated its excellent performance in identifying critical genes regulating mitophagy of osteosarcoma (area under curve [AUC] of ROC: 98.96%; AUC of PR curve: 100%). CERS1 was identified as the most essential gene regulating mitophagy (mean (|SHAP value|): 4.14). Inhibition of CERS1 sensitized cisplatin-resistant osteosarcoma cells to cisplatin, restricting their growth, proliferation, invasion, migration and colony formation and inducing apoptosis. Mechanistically, inhibition of CERS1 restricted mitophagy to destroy the mitochondrial quality control in cisplatin-resistant osteosarcoma cells, including mitochondrial membrane potential loss and unfavourable mitochondrial dynamics, rendering them susceptible to cisplatin-induced apoptosis. More importantly, mitophagy facilitated the immunosuppressive microenvironment formation by significantly modulating T-cell differentiation, adhesion and antigen presentation, and mitophagy mainly affects malignant osteoblasts in the early-mid developmental stage. Immunologically, mitophagy potentially modulated the MIF signalling transmission between malignant osteoblasts and B cells, DCs, CD8+ T cells, NK cells and monocytes through the MIF-(CD74 + CXCR4) receptor-ligand interaction, thereby modulating the biological functions of these immune cells. Collectively, BayeDEM emerged as a promising tool for oncologists to identify pivotal genes governing mitophagy, thereby enabling mitophagy-centric therapeutic strategies to counteract drug resistance.
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Registered trials
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.