Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Inhibition of platelet-tumour cell interaction with ibrutinib reduces proliferation, migration and invasion of lung cancer cells

Zhiqiang Fu¹, Haifeng Wang², Yi Zhou¹, Qi Zhou¹

¹Department of Thoracic Surgery, Shanghai Shidong Hospital, Shanghai, 200438; ²Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Shangai 200433, China.

For correspondence:- Qi Zhou Email: Zhouqicsh@163.com

Accepted: 27 March 2018 Published: 30 April 2018

Citation: Fu Z, Wang H, Zhou Y, Zhou Q. Inhibition of platelet-tumour cell interaction with ibrutinib reduces proliferation, migration and invasion of lung cancer cells. Trop J Pharm Res 2018; 17(4):589-596 doi: 10.4314/tjpr.v17i4.4

© 2018 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the pharmacological role of the Bruton tyrosine kinase (BTK) inhibitor, ibrutinib, in tumour cell-platelet crosstalk in lung cancer.

Methods: Human lung cancer cells A549 were treated with ibrutinib or DMSO. mRNA expression was assessed using reverse transcription-quantitative polymerase chain reaction (RT-PCR), and while western blotting was used to determine protein expression levels. Small interfering RNA (siRNA) transfection was performed to suppress the expression of galectin-3. Colony formation and Transwell® assays were used to determine cell viability, cell invasiveness and migratory ability.

Results: Co-culture of A549 cells and platelets induced activation of BTK/PLCγ2 signalling and subsequent release of PDGF, VEGF and TGFβ1 from de-granulated platelets. However, knocking down of galectin-3 inhibited A549-induced platelet activation. Conversely, platelet activation upregulated the expression of galectin-3 via the release of PDGF. Moreover, ibrutinib significantly (p < 0.05) inhibited cell viability, migration, and invasion.

Conclusion: These results suggest that ibrutinib may be a novel therapeutic treatment for lung cancer

Keywords: Bruton tyrosine kinase, Ibrutinib, Lung cancer, Platelet