ArticlePloS one2011
Versican G3 domain modulates breast cancer cell apoptosis: a mechanism for breast cancer cell response to chemotherapy and EGFR therapy.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Proteoglycans as Molecular Regulators of Bone Metastasis: Extracellular Matrix Remodeling, Tumor-Bone Crosstalk, Dormancy, and Therapeutic Opportunities.Biomolecules · 2026Review
- Integration of ATAC-Seq, Transcriptomic, and Proteomics Reveals the Molecular Mechanism of Intramuscular Fat Deposition and Meat Tenderness Regulation in Pig Breeds.Biomolecules · 2025Article
- Increased levels of versican and insulin-like growth factor 1 in peritumoral mammary adipose tissue are related to aggressiveness in estrogen receptor-positive breast cancer.Molecular medicine (Cambridge, Mass.) · 2024Article
- Review
- Genome-Wide Association Study and FFrontiers in genetics · 2022Article
- Versican and Versican-matrikines in Cancer Progression, Inflammation, and Immunity.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020Review
- Proteoglycans in the Pathogenesis of Hormone-Dependent Cancers: Mediators and Effectors.Cancers · 2020Review
- Targeting of stromal versican by miR-144/199 inhibits multiple myeloma by downregulating FAK/STAT3 signalling.RNA biology · 2020Article
- Dissecting the role of hyaluronan synthases in the tumor microenvironment.The FEBS journal · 2019Review
- Genetic variants in the exon region of versican predict survival of patients with resected early-stage hepatitis B virus-associated hepatocellular carcinoma.Cancer management and research · 2018Article
- Proteoglycans-Biomarkers and Targets in Cancer Therapy.Frontiers in endocrinology · 2018Review
- Versican G1 domain enhances adenoviral-mediated transgene expression and can be modulated by inhibitors of the Janus kinase (JAK)/STAT and Src family kinase pathways.The Journal of biological chemistry · 2017Article
- Temporospatial expression of fibulin-1 after acute spinal cord injury in rats.The journal of spinal cord medicine · 2015Article
- Versican upregulation in Sézary cells alters growth, motility and resistance to chemotherapy.Leukemia · 2015Article
- Insights into the key roles of proteoglycans in breast cancer biology and translational medicine.Biochimica et biophysica acta · 2015Review
- Article
- Verbascoside promotes apoptosis by regulating HIPK2-p53 signaling in human colorectal cancer.BMC cancer · 2014Article
- The wound healing, chronic fibrosis, and cancer progression triad.Physiological genomics · 2014Review
- The motile breast cancer phenotype roles of proteoglycans/glycosaminoglycans.BioMed research international · 2014Review
- Friend or foe: the role of microRNA in chemotherapy resistance.Acta pharmacologica Sinica · 2013Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overexpression of EGFR and versican has been reported in association with breast cancers. Considered oncogenic, these molecules may be attractive therapeutic targets. Possessing anti-apoptotic and drug resistant properties, overexpression of these molecules is accompanied by selective sensitization to the process of apoptosis. In this study, we exogenously expressed a versican G3 construct in breast cancer cell lines and analyzed the effects of G3 on cell viability in fetal bovine serum free conditioned media and evaluated the effects of apoptotic agent C2-ceramide, and chemotherapeutic agents including Docetaxel, Doxorubicin, and Epirubicin. Versican G3 domain enhanced tumor cell resistance to apoptosis when cultured in serum free medium, Doxorubicin, or Epirubicin by up-regulating pERK and GSK-3β (S9P). However, it could be prevented by selective EGFR inhibitor AG 1478 and selective MEK inhibitor PD 98059. Both AG 1478 and PD 98059 enhanced expression of pSAPK/JNK, while selective JNK inhibitor SP 600125 enhanced expression of GSK-3β (S9P). Versican G3 promoted cell apoptosis induced by C2-ceramide or Docetaxel by enhancing expression of pSAPK/JNK and decreasing expression of GSK-3β (S9P), an observation blocked by AG 1478 or SP 6000125. Inhibition of endogenous versican expression by siRNA or reduction of versican G3's expression by linking G3 with 3'UTR prevented G3 modulated cell apoptosis. The dual roles of G3 in modulating breast cancer cell resistance to chemotherapeutic agents may in part explain a potential mechanism for breast cancer cell resistance to chemotherapy and EGFR therapy. The apoptotic effects of chemotherapeutics depend upon the activation and balance of down stream signals in the EGFR pathway. GSK-3β (S9P) appears to function as a key checkpoint in this balance of apoptosis and anti-apoptosis. Investigation and potential consideration of targeting GSK-3β (S9P) merits further study.
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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.