NYC ributed conception, designed the study and wrote the manuscript. HXG carriedouttheexperiments, collected and interpretated the data. XMW carriedouttheexperiments, collect ed and interpretated the data. FYX assisted with study implementation. QR and SHL assisted with study implementation and supervised laboratory procedures. BL carriedouttheexperiments, collected and interpretated the data. LZ supervised laboratory procedures. HZ contributed conception, analyzed the data, and wrote the manuscript. Allauthorsreadandapprovedthefinalmanuscript.”
“Background BAY 63-2521 price pancreatic cancer is a devastating disease; it is the www.selleckchem.com/products/MK-1775.html eighth

most common cause of death (from cancer in both sexes combined) in the World, and is responsible for 227,000 deaths per year [1]. The median survival time after tumour detection is 3-6 months [2], with an all-stage 5-year survival rate of < 5% [3]. Surgery offers the best possibility for survival but at time of diagnosis, only 15% of patients are eligible for resection [4]. The poor outcome is mainly due to difficulties in early detection, lack of an effective treatment and limited understanding of the biological characteristics of this disease. Intrinsic resistance to chemotherapy and radiation

[5] coupled with its early systematic dissemination, local tumour progression and metastatic propensity are associated with pancreatic cancer [6]. The processes involved in tumour cell invasion and metastasis are complex. The ability of cancer cells to degrade Vactosertib and adhere to the basement membrane and metastasise to distant organs is one of the most critical aspects of cancer. Adhesion molecules, such as integrins mediate direct cell-cell recognition and cell-matrix interactions [7] are essential for tumour cell migration [8] and

for basement membrane penetration [9]. In pancreatic cancer, expression of integrins α6β1 Staurosporine cost [10–12] and αvβ3 [13] have previously been associated with invasion in cell lines and tissues. However, contrasting results with respect to tumour type and integrin expression patterns makes it difficult to draw general conclusions on the role of specific integrins. Tumour progression and metastasis are associated with changes in a multitude of integrin signalling cascades. Transformed cancer cells are often characterised by the loss/reduction of integrin expression [14, 15]. Extracellular matrix (ECM)-ligand binding to an integrin initiates signals, which are transmitted via different, yet interconnecting, pathways and elicit various cell functions, such as morphological changes, adhesion, migration and gene activation, all relevant to the metastatic cascade. The surrounding microenvironment and adhesion properties of pancreatic tumours and sub-populations within the tumour may determine which integrins increase or reduce metastasis in particular tumours [16].