ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2020
Enhanced Protein Damage Clearance Induces Broad Drug Resistance in Multitype of Cancers Revealed by an Evolution Drug-Resistant Model and Genome-Wide siRNA Screening.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06900647 (Phase I Study to Evaluate the Safety and Preliminary Efficacy of Bortezomib Combined With Cisplatin in Patients With Recurrent or Metastatic Breast Cancer), which is not on this map. Cited by 15 papers.
What it found
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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.
Phase I Study to Evaluate the Safety and Preliminary Efficacy of Bortezomib Combined With Cisplatin in Patients With Recurrent or Metastatic Breast Cancer
Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Tumor cell intrinsic dsRNA innate immune response triggered by PARP inhibitor is compromised in BRCA1-deficient breast cancer by repressing IRF3.Protein & cell · 2026Article
- Mitochondrial Dysfunction in Apoptosis-Resistant Acute Myeloid Leukemia Cells During a Sterile Inflammatory Response.Biomolecules · 2025Article
- Suppressing protein damage response to overcome multidrug resistance in cancer therapy.Cell discovery · 2025Article
- Augment proteasome inhibitor efficacy activates CD8Cell reports. Medicine · 2025Article
- A robust multiplex-DIA workflow profiles protein turnover regulations associated with cisplatin resistance and aneuploidy.Nature communications · 2025Article
- Proteasome: Role in T Cell Function Regulation.International journal of biological sciences · 2025Review
- Therapeutic Chemoresistance in Ovarian Cancer: Emerging Hallmarks, Signaling Mechanisms and Alternative Pathways.Current medicinal chemistry · 2025Review
- Remodeling the Tumor Immune Environment in Breast Cancer via Bortezomib-based Combination Therapy.International journal of biological sciences · 2025Article
- Human patient derived organoids: an emerging precision medicine model for gastrointestinal cancer research.Frontiers in cell and developmental biology · 2024Review
- UGDH promotes tumor-initiating cells and a fibroinflammatory tumor microenvironment in ovarian cancer.Journal of experimental & clinical cancer research : CR · 2023Article
- Cullin-5 deficiency orchestrates the tumor microenvironment to promote mammary tumor development through CREB1-CCL2 signaling.Science advances · 2023Article
- Patient-Derived Organoids Can Guide Personalized-Therapies for Patients with Advanced Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Activation of FGFR2 Signaling Suppresses BRCA1 and Drives Triple-Negative Mammary Tumorigenesis That is Sensitive to Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Accelerating precision anti-cancer therapy by time-lapse and label-free 3D tumor slice culture platform.Theranostics · 2021Article
- Enhanced Protein Damage Clearance Induces Broad Drug Resistance in Multitype of Cancers Revealed by an Evolution Drug-Resistant Model and Genome-Wide siRNA Screening.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
21 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Resistance to therapeutic drugs occurs in virtually all types of cancers, and the tolerance to one drug frequently becomes broad therapy resistance; however, the underlying mechanism remains elusive. Combining a whole whole-genome-wide RNA interference screening and an evolutionary drug pressure model with MDA-MB-231 cells, it is found that enhanced protein damage clearance and reduced mitochondrial respiratory activity are responsible for cisplatin resistance. Screening drug-resistant cancer cells and human patient-derived organoids for breast and colon cancers with many anticancer drugs indicates that activation of mitochondrion protein import surveillance system enhances proteasome activity and minimizes caspase activation, leading to broad drug resistance that can be overcome by co-treatment with a proteasome inhibitor, bortezomib. It is further demonstrated that cisplatin and bortezomib encapsulated into nanoparticle further enhance their therapeutic efficacy and alleviate side effects induced by drug combination treatment. These data demonstrate a feasibility for eliminating broad drug resistance by targeting its common mechanism to achieve effective therapy for multiple 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.