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Original ArticleOpen Access
The Activation of Platelet Aggregation by Human Cholangiocarcinoma Cells is Mediated Through Thrombin Receptor
Akarasereenont P 
,
AiamsaArd T ,
Chotewuttakorn S ,
Thaworn A
,
AiamsaArd T ,
Chotewuttakorn S ,
Thaworn A TIPSUCHON AIAMSA-ARD, M.Sc. *,
ATHIWAT THAWORN, Cert.,M.S.T.*
Tumor cell induced platelet aggregation (TCIP A) played an importance role in early state
of thrombosis in cancer patients. In addition, TCIPA was recognized as one important step in meta-
static cascade. Cholangiocarcinoma, one of the most common cancers in the north-eastern part
of Thailand, associated with thrombosis was reported. The authors investigated the effects of
cholangiocarcinoma cells on platelet function as measured by platelet aggregation. Primary human
chlolangiocarcinoma (HuCCA) cells were established in our laboratory. Cells were cultured as
standard techniques and grown to confluence until used, after which cells were replaced with fresh
medium (Dulbeco Modified Eargle's Medium, DMEM) without serum for 24, 48 and 72 h. Then,
the conditioned medium (CM) was collected. CM (24, 48 and 72 h) from HuCCA failed to induce
platelet aggregation, whereas, HuCCA pellets induced platelet aggregation and potentiated platelet
aggregation induced by submaximal concentration of thrombin. Interestingly, platelet aggregation
induced by HuCCA was inhibited by hirudin (thrombin receptor antagonist; 10, 20 and 40 U) in a
dose dependent manner. Thus, cholangiocarcinoma cells can induce platelet aggregation in a direct
tumor cell-platelet contact
via
thrombin receptor. Therefore, the use of antiplatelet agents especially
via
thrombin receptors may help to prevent TCIPA or metastasis by CCA.
Key word : Chlolangiocarcinoma, Thrombosis, Platelets, Thrombin, Receptor, Signalling
ATHIWAT THAWORN, Cert.,M.S.T.*
Tumor cell induced platelet aggregation (TCIP A) played an importance role in early state
of thrombosis in cancer patients. In addition, TCIPA was recognized as one important step in meta-
static cascade. Cholangiocarcinoma, one of the most common cancers in the north-eastern part
of Thailand, associated with thrombosis was reported. The authors investigated the effects of
cholangiocarcinoma cells on platelet function as measured by platelet aggregation. Primary human
chlolangiocarcinoma (HuCCA) cells were established in our laboratory. Cells were cultured as
standard techniques and grown to confluence until used, after which cells were replaced with fresh
medium (Dulbeco Modified Eargle's Medium, DMEM) without serum for 24, 48 and 72 h. Then,
the conditioned medium (CM) was collected. CM (24, 48 and 72 h) from HuCCA failed to induce
platelet aggregation, whereas, HuCCA pellets induced platelet aggregation and potentiated platelet
aggregation induced by submaximal concentration of thrombin. Interestingly, platelet aggregation
induced by HuCCA was inhibited by hirudin (thrombin receptor antagonist; 10, 20 and 40 U) in a
dose dependent manner. Thus, cholangiocarcinoma cells can induce platelet aggregation in a direct
tumor cell-platelet contact
via
thrombin receptor. Therefore, the use of antiplatelet agents especially
via
thrombin receptors may help to prevent TCIPA or metastasis by CCA.
Key word : Chlolangiocarcinoma, Thrombosis, Platelets, Thrombin, Receptor, Signalling
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