Abstract
Pancreatic cancer is a common type of cancer with poor prognosis worldwide. Postoperative survival depends on the existence of metastasis. Elucidation of the mechanism underlying cancer progression is important to improve prognosis. The RAS-associated protein RAB5 activates intracellular membrane trafficking, and RAB5 expression is correlated to progression and epithelial mesenchymal transition in various cancers.The expression of RAB5 and E-cadherin in 111 pancreatic cancer samples was investigated by immunohistochemical staining, and the relationship among RAB5 expression, clinicopathological factors, and E-cadherin expression was assessed. Furthermore, RAB5 suppression analysis by siRNA was performed to determine the roles of RAB5 in morphological change, proliferation potency, cell migration ability, and invasiveness of the pancreatic cancer cell line.High RAB5 expression correlated with the presence of lymphatic invasion and venous invasion and low E-cadherin expression. Patients with high RAB5 expression had a poorer prognosis than those with low RAB5 expression. RAB5 suppression in pancreatic cancer cells enhanced E-cadherin expression; changed cell morphology from spindle to round; and inhibited proliferation, invasion, and cell migration.RAB5 contributes to poor prognosis and progression in pancreatic cancer patients. It may be a promising candidate for individualized therapy in refractory pancreatic cancer.
Highlights
Pancreatic cancer is a common type of cancer with poor prognosis worldwide [1]
Fifty (45%) pancreatic cancer specimens were assigned to the low RAB5 expression group and 61 (55%) were assigned to the high RAB5 expression group; 63 (57%) pancreatic cancer specimens were assigned to the high E-cadherin expression group and 48 (43%) were assigned to the low E-cadherin expression group (Figure 1A)
The results indicate that RAB5 expression inversely correlated with E-cadherin levels in only pancreatic cancer parts (Figure 1C)
Summary
Pancreatic cancer is a common type of cancer with poor prognosis worldwide [1]. The 5-year survival rate for pancreatic cancer is approximately 10% [2]. Epithelial to mesenchymal transition (EMT) activates embryonic development and cancer progression [5]. EMT is a complex molecular and cellular program by which epithelial cells shed their differentiated characteristics, i.e., cell adhesion and cellular polarity, and acquire mesenchymal features, including motility, invasiveness, and a heightened resistance to apoptosis. These phenotypes contribute to tumor progression and intra-tumoral heterogeneity [6]. There are reports of an emerging relationship between EMT and cancer stem cells [8]. Zheng et al reported the importance of combining EMT inhibition with chemotherapy for the treatment of pancreatic cancer [9]
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