A monoclonal antibody against basic fibroblast growth factor attenuates cisplatin resistance in lung cancer by suppressing the epithelial-mesenchymal transition.
- Publisher:
- SAGE Publishing
- Publication Type:
- Journal Article
- Citation:
- International Journal of Immunopathology and Pharmacology, 2022, 36, pp. 1-10
- Issue Date:
- 2022
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Hu, P | |
dc.contributor.author | So, K | |
dc.contributor.author | Chen, H | |
dc.contributor.author | Lin, Q | |
dc.contributor.author | Xu, M | |
dc.contributor.author |
Lin, Y |
|
dc.date.accessioned | 2023-07-03T05:46:41Z | |
dc.date.available | 2023-07-03T05:46:41Z | |
dc.date.issued | 2022 | |
dc.identifier.citation | International Journal of Immunopathology and Pharmacology, 2022, 36, pp. 1-10 | |
dc.identifier.issn | 0394-6320 | |
dc.identifier.issn | 2058-7384 | |
dc.identifier.uri | http://hdl.handle.net/10453/171146 | |
dc.description.abstract | Objectives: To investigate the underlying mechanisms of how the basic fibroblast growth factor monoclonal antibody (bFGFmAb) attenuates cisplatin (DDP) resistance in lung cancer using A549 cells and cisplatin-resistant A549 cells (A549/DDP). Methods: Cancer cell proliferation, cell viability, and 50% inhibitory concentration (IC50) of cisplatin were assessed. Transwell assays were utilized to evaluate the invasion activity of tumor cells in response to treatment. Epithelial-to-mesenchymal transition markers and drug resistance proteins were analysed using Western blots. Results: We demonstrate that the bFGFmAb inhibits the proliferation and invasion of both A549 and A549/DDP cells. The bFGFmAb increases cisplatin sensitivity of both A549 and A549/DDP cells as evidenced by an increase in the IC50 of cisplatin in A549 and A549/DDP cells. Furthermore, bFGFmAb significantly increases the expression of E-cadherin, whilst decreasing the expression of N-cadherin and bFGF in both cell lines, thereby showing inhibition of epithelial-to-mesenchymal transition. In addition, we demonstrate that bFGFmAb significantly reduces the expression of the lung resistance protein. Conclusions: Our data suggests that the humanized bFGFmAb is a promising agent to attenuate cisplatin resistance in NSCLC. The underlying mechanism for this effect of bFGFmAb may be associated with the inhibition of epithelial-to-mesenchymal transition and reduced expression of lung resistance protein. | |
dc.format | ||
dc.language | eng | |
dc.publisher | SAGE Publishing | |
dc.relation.ispartof | International Journal of Immunopathology and Pharmacology | |
dc.relation.isbasedon | 10.1177/03946320221105134 | |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.subject | 1115 Pharmacology and Pharmaceutical Sciences | |
dc.subject.classification | Immunology | |
dc.subject.mesh | Antibodies, Monoclonal | |
dc.subject.mesh | Cisplatin | |
dc.subject.mesh | Drug Resistance, Neoplasm | |
dc.subject.mesh | Epithelial-Mesenchymal Transition | |
dc.subject.mesh | Fibroblast Growth Factor 2 | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Lung Neoplasms | |
dc.subject.mesh | Antibodies, Monoclonal | |
dc.subject.mesh | Cisplatin | |
dc.subject.mesh | Drug Resistance, Neoplasm | |
dc.subject.mesh | Epithelial-Mesenchymal Transition | |
dc.subject.mesh | Fibroblast Growth Factor 2 | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Lung Neoplasms | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Lung Neoplasms | |
dc.subject.mesh | Cisplatin | |
dc.subject.mesh | Fibroblast Growth Factor 2 | |
dc.subject.mesh | Antibodies, Monoclonal | |
dc.subject.mesh | Drug Resistance, Neoplasm | |
dc.subject.mesh | Epithelial-Mesenchymal Transition | |
dc.subject.mesh | Antibodies, Monoclonal | |
dc.subject.mesh | Cisplatin | |
dc.subject.mesh | Drug Resistance, Neoplasm | |
dc.subject.mesh | Epithelial-Mesenchymal Transition | |
dc.subject.mesh | Fibroblast Growth Factor 2 | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Lung Neoplasms | |
dc.title | A monoclonal antibody against basic fibroblast growth factor attenuates cisplatin resistance in lung cancer by suppressing the epithelial-mesenchymal transition. | |
dc.type | Journal Article | |
utslib.citation.volume | 36 | |
utslib.location.activity | England | |
utslib.for | 1115 Pharmacology and Pharmaceutical Sciences | |
pubs.organisational-group | /University of Technology Sydney | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science/School of Life Sciences | |
utslib.copyright.status | open_access | * |
pubs.consider-herdc | false | |
dc.date.updated | 2023-07-03T05:46:38Z | |
pubs.publication-status | Published | |
pubs.volume | 36 |
Abstract:
Objectives: To investigate the underlying mechanisms of how the basic fibroblast growth factor monoclonal antibody (bFGFmAb) attenuates cisplatin (DDP) resistance in lung cancer using A549 cells and cisplatin-resistant A549 cells (A549/DDP). Methods: Cancer cell proliferation, cell viability, and 50% inhibitory concentration (IC50) of cisplatin were assessed. Transwell assays were utilized to evaluate the invasion activity of tumor cells in response to treatment. Epithelial-to-mesenchymal transition markers and drug resistance proteins were analysed using Western blots. Results: We demonstrate that the bFGFmAb inhibits the proliferation and invasion of both A549 and A549/DDP cells. The bFGFmAb increases cisplatin sensitivity of both A549 and A549/DDP cells as evidenced by an increase in the IC50 of cisplatin in A549 and A549/DDP cells. Furthermore, bFGFmAb significantly increases the expression of E-cadherin, whilst decreasing the expression of N-cadherin and bFGF in both cell lines, thereby showing inhibition of epithelial-to-mesenchymal transition. In addition, we demonstrate that bFGFmAb significantly reduces the expression of the lung resistance protein. Conclusions: Our data suggests that the humanized bFGFmAb is a promising agent to attenuate cisplatin resistance in NSCLC. The underlying mechanism for this effect of bFGFmAb may be associated with the inhibition of epithelial-to-mesenchymal transition and reduced expression of lung resistance protein.
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