Platelet induced hepatocellular carcinoma HEPG2 cell proliferation and angiogenic potential is integrin IIb3 dependent.

Conference poster


Rashed, Al-Hammad, Anene, C., Graham, A.M. and Roberts, W. (2015). Platelet induced hepatocellular carcinoma HEPG2 cell proliferation and angiogenic potential is integrin IIb3 dependent. Taylor & Francis. https://doi.org/10.3109/09537104.2015.1115703
AuthorsRashed, Al-Hammad, Anene, C., Graham, A.M. and Roberts, W.
TypeConference poster
Abstract

Hepatocellular carcinoma (HCC) is the fifth most common malignancy in the world, leading to an estimated one million deaths annually. Although several treatment options are available, the prognosis for HCC patients remains poor, largely due to rapid metastasis. Liver cancers are often highly vascularized, and both experimental and clinical data indicate that the progression of HCC is associated with increased angiogenesis, aiding in their metastatic potential. The vascular nature of HCCs gives them ample opportunity to recruit and interact with platelets. Platelets bind to cancer cells through a range of receptors including the integrin aIIbb3, which is upregulated by platelet derived ADP and thromboxane A2 (TxA2). When activated, platelets release a large array of cytokines and growth factors that may induce angiogenesis and aid in the migration, invasion and proliferation of a range of tumour cells, but it is unclear if they support HCC progression. Identifying the roles platelets play in enhancing HCC proliferation and metastatic potential could provide novel treatment strategies to target HCC.

Year2015
JournalPlatelets
PublisherTaylor & Francis
ISSN1369-1635
Digital Object Identifier (DOI)https://doi.org/10.3109/09537104.2015.1115703
Accepted author manuscript
License
File Access Level
Open
Publication dates
Print15 Dec 2015
Publication process dates
Deposited21 Jun 2022
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https://openresearch.lsbu.ac.uk/item/8zyq6

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Accepted author manuscript
Anene, C.A., Graham, A., Boyne, J. and Roberts, W., 2019b.pdf
License: CC BY 4.0
File access level: Open

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