ArticleNature communications2020
Enhancing chemotherapy response through augmented synthetic lethality by co-targeting nucleotide excision repair and cell-cycle checkpoints.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 48 citations in OpenAlex.
- XPA lactylation is required for UV-induced DNA damage repair.Nucleic acids research · 2026Article
- NSUN2-mediated m5C modification of E2F1 promotes lung adenocarcinoma progression via the RAD54L signaling axis.Respiratory research · 2026Article
- Suppressing protein damage response to overcome multidrug resistance in cancer therapy.Cell discovery · 2025Article
- Elucidating the potential of EGFR mutated NSCLC and identifying its multitargeted inhibitors.Scientific reports · 2025Article
- S6K1 is a Targetable Vulnerability in Tumors Exhibiting Plasticity and Therapy Resistance.International journal of biological sciences · 2025Article
- GG-NER's role in androgen receptor signaling inhibitor response for advanced prostate cancer.Cell communication and signaling : CCS · 2024Article
- Loss of MK2 Enhances Radiation-Mediated Apoptosis in Bladder Cancer.World journal of oncology · 2024Article
- Genetic influence of meningioma on cisplatin resistance: a Mendelian randomization analysis.International journal of clinical pharmacy · 2024Article
- Synthesis of a light-responsive platinum curcumin complex, chemical and biological investigations and delivery to tumor cells by means of polymeric nanoparticles.Nanoscale advances · 2023Article
- Constitutively Synergistic Multiagent Drug Formulations Targeting MERTK, FLT3, and BCL-2 for Treatment of AML.Pharmaceutical research · 2023Article
- Development of constitutively synergistic nanoformulations to enhance chemosensitivity in T-cell leukemia.Journal of controlled release : official journal of the Controlled Release Society · 2023Article
- Biphasic JNK-Erk signaling separates the induction and maintenance of cell senescence after DNA damage induced by topoisomerase II inhibition.Cell systems · 2023Article
- A nuclease-mimetic platinum nanozyme induces concurrent DNA platination and oxidative cleavage to overcome cancer drug resistance.Nature communications · 2022Article
- Response of the Urothelial Carcinoma Cell Lines to Cisplatin.International journal of molecular sciences · 2022Article
- Phospholipase A/acyltransferase 4 is a prognostic biomarker and correlated with immune infiltrates in pancreatic cancer.Heliyon · 2022Article
- Cisplatin resistance-related multi-omics differences and the establishment of machine learning models.Journal of translational medicine · 2022Article
- Nanomedicine Strategies for Management of Drug Resistance in Lung Cancer.International journal of molecular sciences · 2022Review
- Mitogen-activated protein kinase-activated protein kinase-2 (MK2) and its role in cell survival, inflammatory signaling, and migration in promoting cancer.Molecular carcinogenesis · 2022Article
- Proteins from the DNA Damage Response: Regulation, Dysfunction, and Anticancer Strategies.Cancers · 2021Review
- MK2 degradation as a sensor of signal intensity that controls stress-induced cell fate.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
Corrections and comments
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Authors and funding
18 authors at 8 institutions in 3 countries.
Funding
Abstract
In response to DNA damage, a synthetic lethal relationship exists between the cell cycle checkpoint kinase MK2 and the tumor suppressor p53. Here, we describe the concept of augmented synthetic lethality (ASL): depletion of a third gene product enhances a pre-existing synthetic lethal combination. We show that loss of the DNA repair protein XPA markedly augments the synthetic lethality between MK2 and p53, enhancing anti-tumor responses alone and in combination with cisplatin chemotherapy. Delivery of siRNA-peptide nanoplexes co-targeting MK2 and XPA to pre-existing p53-deficient tumors in a highly aggressive, immunocompetent mouse model of lung adenocarcinoma improves long-term survival and cisplatin response beyond those of the synthetic lethal p53 mutant/MK2 combination alone. These findings establish a mechanism for co-targeting DNA damage-induced cell cycle checkpoints in combination with repair of cisplatin-DNA lesions in vivo using RNAi nanocarriers, and motivate further exploration of ASL as a generalized strategy to improve cancer treatment.
Indexed as
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What OpenQuestion holds
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.