PhD Scientific Days 2026

Poster Session 2.B - Molecular Medicine

Platelet SYK promotes solid tumor metastasis via TXA2-mediated immunosuppression

Előadó neve

Sándor, Luca, MSc

Neptune code

eij2nn

Előadó munkahelye

Élettani Intézet

Előadó telefonszáma

+36301817993

Előadó e-mail címe

sandor.luca@phd.semmelweis.hu

Az előadás címe

Platelet SYK promotes solid tumor metastasis via TXA2-mediated immunosuppression

Szerző(k) neve és munkahelye

Luca Sándor¹

1: Élettani Intézet

Bemutatás módja

Poszter

Szekció

Poster Session 2.B - Molecular Medicine

Language of the presentation

Hungarian

Preferred session

Molecular Medicine

Összefoglaló szövege

Introduction
Metastasis is the leading cause of cancer-related mortality and involves complex interactions between tumor and host cells. Platelets are increasingly recognized as key contributors to tumor dissemination, yet the molecular mechanisms underlying platelet activation in metastasis remain incompletely understood.
Aims
To investigate the role of platelet spleen tyrosine kinase (SYK) in solid tumor metastasis and to understand the underlying mechanisms, we focused on deciphering the role of platelet SYK in tumor immunosuppression.
Methods
Platelet-specific SYK-deficient mice (SykΔPlt) and wild-type controls were used in malignant melanoma (B16F10) and colorectal carcinoma (MC38) metastasis models. Pharmacological SYK inhibitors (fostamatinib, entospletinib, lanraplenib) and TXA2 synthase inhibitor (Y-20811) were applied. Metastasis formation was assessed by histological processing of lung and intestine tissues. Platelet numbers and function, TXA2/TXB2 levels, and CD8+ T cell responses were analyzed using in vitro co-culture systems, ELISA and flow cytometry.
Results
Genetic deletion or pharmacological inhibition of SYK significantly reduced metastatic burden without affecting primary tumor growth in animal models of metastasis. SYK-expressing platelets secreted TXA2, whereas SYK-deficient platelets showed impaired TXA2 release. Reduced TXA2 levels correlated with increased CD8+ T cell numbers and activity. Mechanistically, platelet-derived TXA2 suppressed CD8+ T cell proliferation and IFN-γ production in a contact-independent manner. Administration of a TXA2 analogue restored metastasis formation in SYK-deficient mice, while inhibition of TXA2 production mimicked the anti-metastatic effects of SYK inhibition.
Conclusion
Platelet SYK drives solid tumor metastasis by promoting TXA2-mediated immunosuppression of CD8+ T cells. Targeting the SYK–TXA2 axis may represent a promising therapeutic strategy to enhance anti-tumor immunity and limit metastatic progression.
Funding
Supported by the Hungarian National Research, Development and Innovation Office (TKP-EGA-29), the János Bolyai Research Scholarship, the Semmelweis 250+ Scholarship, and the Cooperative Translational Research Program of Semmelweis University.

University

Semmelweis University

Supervisor

Dr. Győri Dávid

Publication of my abstract

I give consent to the publication of my abstract on the website of the congress.

phd.section.field

in doctoral studies after complex exam (PhD)

Kind

Szabad

Status

elfogadva

Accepted presentation method

poszter

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

8038

Start

19:06

End

19:09