ArticleThe Journal of clinical investigation2019
Hsp90B enhances MAST1-mediated cisplatin resistance by protecting MAST1 from proteosomal degradation.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 42 citations in OpenAlex.
- HSP90 shields ROC1/RBX1 from proteasomal degradation by CHIP E3 ubiquitin ligase to promote lung adenocarcinoma.Signal transduction and targeted therapy · 2026Article
- Oxidative stress-driven mRedox biology · 2026Article
- Targeting HSP90 in cancer: advances in the development of inhibitors, mechanisms of action, and therapeutic applications.Molecular cancer · 2026Review
- Small-molecule inhibitor of C‑terminal HSP90 dimerization modulates autophagy and functions synergistically with mTOR inhibition to kill cisplatin-resistant cancer cells.Cell death & disease · 2025Article
- Divergent oncogenic signaling and immune microenvironment changes in low-grade serous ovarian cancer patients undergoing intraperitoneal chemotherapy.NPJ precision oncology · 2025Article
- RNA sequencing and bioinformatics analysis have identifiedTranslational cancer research · 2025Article
- MAST Kinases' Function and Regulation: Insights from Structural Modeling and Disease Mutations.Biomedicines · 2025Article
- ACAT1-Mediated ME2 Acetylation Drives Chemoresistance in Ovarian Cancer by Linking Glutaminolysis to Lactate Production.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- circTP63-N suppresses the proliferation and metastasis of nasopharyngeal carcinoma via engaging with HSP90AB1 to modulate the YAP1/Hippo signaling pathway.Science China. Life sciences · 2025Article
- mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Drug resistance mechanisms and treatment strategies mediated by Ubiquitin-Specific Proteases (USPs) in cancers: new directions and therapeutic options.Molecular cancer · 2024Review
- An update on the secretory functions of brown, white, and beige adipose tissue: Towards therapeutic applications.Reviews in endocrine & metabolic disorders · 2024Review
- USP28 promotes tumorigenesis and cisplatin resistance by deubiquitinating MAST1 protein in cancer cells.Cellular and molecular life sciences : CMLS · 2024Article
- HSP90 inhibition suppresses tumor glycolytic flux to potentiate the therapeutic efficacy of radiotherapy for head and neck cancer.Science advances · 2024Article
- Prospective Identification of Prognostic Hot-Spot Mutant Gene Signatures for Leukemia: A Computational Study Based on Integrative Analysis of TCGA and cBioPortal Data.Molecular biotechnology · 2023Article
- Microtubule-Associated Serine/Threonine (MAST) Kinases in Development and Disease.International journal of molecular sciences · 2023Review
- Protein degradation: expanding the toolbox to restrain cancer drug resistance.Journal of hematology & oncology · 2023Review
- ODF2L acts as a synthetic lethal partner with WEE1 inhibition in epithelial ovarian cancer models.The Journal of clinical investigation · 2023Article
- Article
- Multi-omic profiling reveals the ataxia protein sacsin is required for integrin trafficking and synaptic organization.Cell reports · 2022Article
Corrections and comments
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Authors and funding
17 authors at 2 institutions in 1 country.
Funding
Abstract
Microtubule-associated serine/threonine kinase 1 (MAST1) is a central driver of cisplatin resistance in human cancers. However, the molecular mechanism regulating MAST1 levels in cisplatin-resistant tumors is unknown. Through a proteomics screen, we identified the heat shock protein 90 B (hsp90B) chaperone as a direct MAST1 binding partner essential for its stabilization. Targeting hsp90B sensitized cancer cells to cisplatin predominantly through MAST1 destabilization. Mechanistically, interaction of hsp90B with MAST1 blocked ubiquitination of MAST1 at lysines 317 and 545 by the E3 ubiquitin ligase CHIP and prevented proteasomal degradation. The hsp90B-MAST1-CHIP signaling axis and its relationship with cisplatin response were clinically validated in cancer patients. Furthermore, combined treatment with a hsp90 inhibitor and the MAST1 inhibitor lestaurtinib further abrogated MAST1 activity and consequently enhanced cisplatin-induced tumor growth arrest in a patient-derived xenograft model. Our study not only uncovers the regulatory mechanism of MAST1 in tumors but also suggests a promising combinatorial therapy to overcome cisplatin resistance in human cancers.
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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.