BACKGROUND : Platelets are known contributors to the vascularization, metastasis and growth of tumors. Upon their
interaction with cancer cells they are activated resulting in degranulation and release of constituents. Since the apoptotic-
and autophagic effects of 2-ethyl-3-O-sulphamoyl-estra-1,3,5(10)16-tetraene (ESE-16) has been shown to occur
in vitro and this compound was designed to bind to carbonic anhydrase II (CAII), the possible occurrence of these cell
death mechanisms in platelets as circulatory components, is of importance.
METHODS : Scanning electron microscopy was used to assess morphological changes in platelets after exposure to
ESE-16. The possible apoptotic- and autophagic effect of ESE-16 in platelets was also determined by means of flow
cytometry through measurement of Annexin V-FITC, caspase 3 activity, autophagy related protein 5 levels and light
chain 3-I to light chain 3-II conversion.
RESULTS : Scanning electron microscopy revealed no changes in ESE-16-treated platelets when compared to vehicletreated
samples. Apoptosis detection by Annexin V-FITC and measurement of caspase 3 activity indicated that there
was no increase in apoptosis when platelets were exposed to ESE-16. The incidence of autophagy by measurement
of autophagy related protein 5 levels and light chain 3-I to light chain 3-II conversion showed that exposure to ESE-16
did not cause the incidence of autophagy in platelets.
CONCLUSION : This is the first ex vivo study reporting on involvement of apoptosis- and autophagy-related targets in
platelets after exposure to ESE-16, warranting further investigation in platelets of cancer patients.