ArticleScientific reports2017
Phosphoproteomics Reveals HMGA1, a CK2 Substrate, as a Drug-Resistant Target in Non-Small Cell Lung Cancer.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- HMGA proteins in the nervous system: role in brain tumorigenesis and neurodegeneration.Cell death discovery · 2026Review
- The role of HMGA1 in genome stability: Implications in human cancer.Cellular and molecular life sciences : CMLS · 2026Review
- Phosphoproteomic analysis reveals the diversity of signaling behind ErbB-inhibitor-induced phenotypes.The FEBS journal · 2025Article
- Chemotherapy enhances HMGA1 secretion through the mutant p53-CK2 axis in pancreatic ductal adenocarcinoma cells.Cell death & disease · 2025Article
- FAIM modulates HCC progression via enhancing HMGA1 interaction with CDK7 and promoting its phosphorylation level.Journal of translational medicine · 2025Article
- Advancements in Global Phosphoproteomics Profiling: Overcoming Challenges in Sensitivity and Quantification.Proteomics · 2025Review
- Application of omics in the diagnosis, prognosis, and treatment of acute myeloid leukemia.Biomarker research · 2024Review
- Article
- PROTEOMAS: a workflow enabling harmonized proteomic meta-analysis and proteomic signature mapping.Journal of cheminformatics · 2023Article
- Article
- HMGA1 gene expression level in cancer tissue and blood samples of non-small cell lung cancer (NSCLC) patients: preliminary report.Molecular genetics and genomics : MGG · 2022Article
- Prognostic Significance ofInternational journal of molecular sciences · 2022Article
- Phosphoproteomics profiling reveals a kinase network conferring acute myeloid leukaemia intrinsic chemoresistance and indicates HMGA1 phosphorylation as a potential influencer.Clinical and translational medicine · 2022Article
- Motif-centric phosphoproteomics to target kinase-mediated signaling pathways.Cell reports methods · 2022Article
- Oncogenic Role of Exosomal Circular and Long Noncoding RNAs in Gastrointestinal Cancers.International journal of molecular sciences · 2022Review
- High Mobility Group A1 (HMGA1): Structure, Biological Function, and Therapeutic Potential.International journal of biological sciences · 2022Review
- Radiomics and gene expression profile to characterise the disease and predict outcome in patients with lung cancer.European journal of nuclear medicine and molecular imaging · 2021Observational
- Elevating CDCA3 Levels Enhances Tyrosine Kinase Inhibitor Sensitivity in TKI-Resistant EGFR Mutant Non-Small-Cell Lung Cancer.Cancers · 2021Article
- HMGA1, Moonlighting Protein Function, and Cellular Real Estate: Location, Location, Location!Biomolecules · 2021Review
- The origin of the expressed retrotransposed gene ACTBL2 and its influence on human melanoma cells' motility and focal adhesion formation.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although EGFR tyrosine kinase inhibitors (TKIs) have demonstrated good efficacy in non-small-cell lung cancer (NSCLC) patients harboring EGFR mutations, most patients develop intrinsic and acquired resistance. We quantitatively profiled the phosphoproteome and proteome of drug-sensitive and drug-resistant NSCLC cells under gefitinib treatment. The construction of a dose-dependent responsive kinase-substrate network of 1548 phosphoproteins and 3834 proteins revealed CK2-centric modules as the dominant core network for the potential gefitinib resistance-associated proteins. CK2 knockdown decreased cell survival in gefitinib-resistant NSCLCs. Using motif analysis to identify the CK2 core sub-network, we verified that elevated phosphorylation level of a CK2 substrate, HMGA1 was a critical node contributing to EGFR-TKI resistance in NSCLC cell. Both HMGA1 knockdown or mutation of the CK2 phosphorylation site, S102, of HMGA1 reinforced the efficacy of gefitinib in resistant NSCLC cells through reactivation of the downstream signaling of EGFR. Our results delineate the TKI resistance-associated kinase-substrate network, suggesting a potential therapeutic strategy for overcoming TKI-induced resistance in NSCLC.
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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.