ArticleOncogene2022
Menin inhibition suppresses castration-resistant prostate cancer and enhances chemosensitivity.
Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- HSP27 functional switch drives castration-resistant prostate cancer via mTOR pathway activation, highlighting promising combination therapies.Journal of experimental & clinical cancer research : CR · 2026Article
- Menin-driven mTOR signaling sustains taxane resistance in CRPC and reveals a targetable vulnerability for combination therapy.Cell communication and signaling : CCS · 2025Article
- Chromatin-focused genetic and chemical screens identify BRPF1 as a targetable vulnerability in Taxol-resistant triple-negative breast cancer.Experimental & molecular medicine · 2025Article
- Menin: from molecular insights to clinical impact.Epigenomics · 2025Review
- Histone-modifying enzymes as drivers and therapeutic targets in androgen-resistant prostate cancer.Frontiers in endocrinology · 2025Review
- Identification of epithelial-mesenchymal transition prognostic signature associated with prognosis, tumor microenvironment, and therapeutic effect in prostate cancer.Frontiers in genetics · 2025Article
- Targeting Menin in Acute Myeloid Leukemia: Therapeutic Advances and Future Directions.Cancers · 2024Review
- Unmasking Neuroendocrine Prostate Cancer with a Machine Learning-Driven Seven-Gene Stemness Signature That Predicts Progression.International journal of molecular sciences · 2024Article
- Unmasking Neuroendocrine Prostate Cancer with a Machine Learning-Driven 7-Gene Stemness Signature that Predicts Progression.medRxiv : the preprint server for health sciences · 2024Article
- Menin in Cancer.Genes · 2024Review
- An Overview of Altered Pathways Associated with Sensitivity to Platinum-Based Chemotherapy in Neuroendocrine Tumors: Strengths and Prospects.International journal of molecular sciences · 2024Review
- Unveiling potential: urinary exosomal mRNAs as non-invasive biomarkers for early prostate cancer diagnosis.BMC urology · 2024Article
- Castration-Resistant Prostate Cancer: From Uncovered Resistance Mechanisms to Current Treatments.Cancers · 2023Review
- The heat shock protein Hsp27 controls mitochondrial function by modulating ceramide generation.Cell reports · 2023Article
- Article
- Senescent CD8Cancer science · 2023Article
- DDX5 mRNA-targeting antisense oligonucleotide as a new promising therapeutic in combating castration-resistant prostate cancer.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Evaluating the role of MEN1 gene expression and its clinical significance in breast cancer patients.PloS one · 2023Article
- Combinatorial targeting of menin and the histone methyltransferase DOT1L as a novel therapeutic strategy for treatment of chemotherapy-resistant ovarian cancer.Cancer cell international · 2022Article
- HSP27/Menin Expression as New Prognostic Serum Biomarkers of Prostate Cancer Aggressiveness Independent of PSA.Cancers · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
18 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disease progression and therapeutic resistance of prostate cancer (PC) are linked to multiple molecular events that promote survival and plasticity. We previously showed that heat shock protein 27 (HSP27) acted as a driver of castration-resistant phenotype (CRPC) and developed an oligonucleotides antisense (ASO) against HSP27 with evidence of anti-cancer activity in men with CRPC. Here, we show that the tumor suppressor Menin (MEN1) is highly regulated by HSP27. Menin is overexpressed in high-grade PC and CRPC. High MEN1 mRNA expression is associated with decreased biochemical relapse-free and overall survival. Silencing Menin with ASO technology inhibits CRPC cell proliferation, tumor growth, and restores chemotherapeutic sensitivity. ChIP-seq analysis revealed differential DNA binding sites of Menin in various prostatic cells, suggesting a switch from tumor suppressor to oncogenic functions in CRPC. These data support the evaluation of ASO against Menin for CRPC.
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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.