PB1422 - Interaction of tumor cells A549 and OKP-GS with platelets and platelet derived components influence tumor cell proliferation as well as tumor-cell induced platelet aggregation

Tuesday, June 25, 2024

13:45 – 14:45 ICT

Room: Exhibition Hall

Co-Author(s)

VS

Vladislav A. Shumskiy

Junior researcher
Institute of Biophysics and Cell Engineering NAS of Belarus
Minsk, Minskaya Voblasts', Belarus
UK

Ulia D. Korol

Junior researcher
Institute of Biophysics and Cell Engineering NAS of Belarus
Minsk, Minskaya Voblasts', Belarus
Anatoli U. Kokhan

Junior researcher
Institute of biophysics and cell engeneering of NAS of Belarus
Minsk, Minskaya Voblasts', Belarus
Tatsiana G. Dubouskaya, PhD

senior researcher
Institute of biophysics and cell engineering NAS of Belarus
Minsk, Minskaya Voblasts', Belarus
AS

Anastasia N. Sveshnikova

Head of Laboratory
Dmitry Rogachev National Medical Research Center Of Pediatric Hematology, Oncology and Immunology, Moscow, Russia
Moscow, Moskva, Russia

Presenting Author(s)

Ekaterina V. Shamova, PhD

Head of Laboratory of Medical Biophysics
Institute of biophysics and cell engineering NAS of Belarus, Minsk, Belarus
Minsk, Minskaya Voblasts', Belarus

Background: Today there is strong evidence that platelets are involved in cancer progression and metastasis. Platelets interact with tumor cells by various mechanisms and their impact on cancer progression depends on cancer type.

Aims: In present study we have investigated the influence of platelets and their components (microvesicles (MVs), lysate, secretome) on tumor cell (OKP-GS - kidney carcinoma, A549 -lung carcinoma) proliferation and their ability to induce platelet aggregation (TCIPA).

Methods: Platelets were isolated from citrate-stabilized peripheral blood. Platelet MVs and lysate were obtained by sequential centrifugation of thrombin-stimulated platelets. Lysate was obtained by freeze/thaw cycles of platelets. Cell cultures were grown in DMEM with 10% fetal bovine serum (FBS) or 5% platelet secretome or 10% lysate. Tumor cell proliferation was assessed using CyQUANT kit. TCIPA was registered by optical aggregometry and assessed by lag-period and extent of aggregation. All experiments were performed in accordance with Helsinki Declaration.

Results: Washed platelets (2x104-2x105), platelet MVs and secretome, incubated with tumor cells for 48 hours, enhanced proliferation of OKP-GS but reduced the proliferation of A549 cells. A549 cells became elongated and obtained stromal- appearance that indicated epithelial-mesenchymal transition (EMT). TCIPA was observed for both cell lines but only in the presence of blood plasma (0.1-1.0 %) and was fully inhibited by heparin, suggesting the role of tissue factor (TF) in this process. Tumor cell cultivation with platelet secretome or lysate instead of FBS influenced TCIPA depending on tumor cell type: reduced OKP-GS/TCIPA and enhanced A549/TCIPA.

Conclusion(s): Our data indicate that platelet contribution to tumor progression and metastasis may depend on tumor cell type. Whereas platelets can promote EMT and TCIPA for lung carcinoma tumor cells, the impact of platelets on kidney carcinoma progression may be due to stimulation of tumor cell proliferative activity.
This work is supported by grant B23-RSF162 and grant 23-45-10039.