Surface Expressions of Platelet Glycoprotein Ibα, GpIIb/IIIa, and P-Selectin Are Elevated in Lung Cancer Patients

Thromboembolic events are common symptoms in patients with cancer, and the mechanisms are not totally understood. The platelet adhesion moleculars play important roles in the process of thrombus formation. The aim of the current study is to investigate the surface expression of platelet glycoprotein (GP) Ibα, GPIIb/IIIa, and P-selectin in patients with lung cancer.

Platelets were isolated from patients with lung cancer and normal volunteers, and then the surface expressions of platelet GP Ibα, GPIIb/IIIa, and P-selectin were measured by Flow cytometry. The glycocalicin (GC) fragments in the peripheral blood of patients with lung cancer were tested by Western blot. The surface expression of GP Ibα on normal volunteers' platelets incubated with the platelet-poor plasma (PPP) of patients with lung cancer was measured by Flow cytometry and Western blot.

The surface expressions of platelet GP Ibα, GPIIb/IIIa, and P-selectin were obviously increased in patients with lung cancer compared with that of normal volunteers, and the GC fragments in PPP were also increased in patients with lung cancer. Incubation of control platelets with the PPP from cancer patients resulted in the elevation of the surface expression of GP Ibα in control platelets. Furthermore, the expressions of GP Ibα, GPIIb/IIIa, and P-selectin on platelets from patients with advanced stage of lung cancer (III-IV stage) were significantly higher than those with early stage (I-II stage) (P<0.05). However, there were not significantly difference in the surface expressions of GP Ibα, GPIIb/IIIa, and P-selectin among the pathological types of lung cancer (squamous cell carcinoma, adenocarcinoma, small cell lung carcinoma, large cell lung carcinoma) (P>0.05).

The surface expressions of platelet GP Ibα, GPIIb/IIIa, and P-selectin were obviously elevated in patients with lung cancer, and the plasma from cancer patients is responsible for the elevations. These findings provide a new view to understand the pathogenic mechanisms of thromboembolic events in the patients with lung cancer.

No relevant conflicts of interest to declare.