ArticleMolecular oncology2017
Heat-shock protein 27 (HSP27, HSPB1) is synthetic lethal to cells with oncogenic activation of MET, EGFR and BRAF.
Article in Molecular oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 33 citations in OpenAlex.
- Ac-SDKP modulates apoptosis via HSP27 and the FAS/FASL and mitochondrial axes.Animal models and experimental medicine · 2026Article
- Review
- Honokiol Inhibits Colorectal Cancer Cell Growth: Involvement of Hsp27 as a Molecular Target.Current issues in molecular biology · 2025Article
- Two-Dimensional Polyacrylamide Gel Electrophoresis Coupled with Nanoliquid Chromatography-Tandem Mass Spectrometry-Based Identification of Differentially Expressed Proteins and Tumorigenic Pathways in the MCF7 Breast Cancer Cell Line Transfected for Jumping Translocation Breakpoint Protein Overexpression.International journal of molecular sciences · 2023Article
- The heat shock protein Hsp27 controls mitochondrial function by modulating ceramide generation.Cell reports · 2023Article
- Activation of the HSP27-AKT axis contributes to gefitinib resistance in non-small cell lung cancer cells independent of EGFR mutations.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- The Chaperone System in Breast Cancer: Roles and Therapeutic Prospects of the Molecular Chaperones Hsp27, Hsp60, Hsp70, and Hsp90.International journal of molecular sciences · 2022Review
- Atractylenolide I inhibits EMT and enhances the antitumor effect of cabozantinib in prostate cancerFrontiers in oncology · 2022Article
- Novel characterization discoveries of ferroptosis-associated molecules in COAD microenvironment based TCGA data.Frontiers in molecular biosciences · 2022Article
- Overexpressed DEPDC1B contributes to the progression of hepatocellular carcinoma by CDK1.Aging · 2021Article
- Androgen receptor (AR) antagonism triggers acute succinate-mediated adaptive responses to reactivate AR signaling.EMBO molecular medicine · 2021Article
- Use of four genes in exosomes as biomarkers for the identification of lung adenocarcinoma and lung squamous cell carcinoma.Oncology letters · 2021Article
- Small Heat Shock Proteins in Cancers: Functions and Therapeutic Potential for Cancer Therapy.International journal of molecular sciences · 2020Review
- Article
- Specific Roles of HSP27 S15 Phosphorylation Augmenting the Nuclear Function of HER2 to Promote Trastuzumab Resistance.Cancers · 2020Article
- Ivermectin inhibits HSP27 and potentiates efficacy of oncogene targeting in tumor models.The Journal of clinical investigation · 2020Article
- The Association Between Heat-Shock Protein Polymorphisms and Prognosis in Lung Cancer Patients Treated With Platinum-Based Chemotherapy.Frontiers in pharmacology · 2020Article
- HSP27 promotes epithelial-mesenchymal transition through activation of the β-catenin/MMP3 pathway in pancreatic ductal adenocarcinoma cells.Translational cancer research · 2019Article
- Gene expression alterations of human liver cancer cells following borax exposure.Oncology reports · 2019Article
- Runx2 stimulates neoangiogenesis through the Runt domain in melanoma.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The small heat-shock protein of 27 kDa (HSP27) is highly expressed in many cancers and is associated with aggressive tumour behaviour, metastasis, poor prognosis and resistance to chemotherapy. We aimed at assessing the role of HSP27 in modulating responses to target therapies. We selected several oncogene-addicted cancer cell lines, which undergo either cell cycle blockade or cell death in response to agents that target the specific oncogene. Surprisingly, HSP27 suppression alone resulted in the apoptotic death of MET-addicted EBC-1 lung cancer cells, epidermal growth factor receptor (EGFR)-addicted colorectal carcinoma (CRC) DiFi cells and BRAF-addicted CRC COLO205 and OXCO-1 and melanoma COLO741 cells, all of which also undergo death when treated with the specific targeted agent. In other cell lines, such as MET-addicted gastric carcinoma MKN45 and EGFR-addicted CRC SW48 lines, where oncogene inhibition only blocked proliferation, HSP27 knockdown made targeted agents switch from cytostatic to cytotoxic activity. Mechanistically, the more the cells were susceptible to HSP27 suppression, the more they were primed for death, as demonstrated by increased levels of mitochondrial outer membrane permeabilization. Priming for death was accompanied by the increase in pro-apoptotic proteins of the BCL2 family and of active caspase-3 and lamin B. Together, these data suggest that oncogene-addicted cells require HSP27 for survival and that HSP27 might interfere with the effectiveness of targeted agents.
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