alexa RAN GTPase and Osteopontin in Pancreatic Cancer
ISSN: 2165-7092

Pancreatic Disorders & Therapy
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Research Article

RAN GTPase and Osteopontin in Pancreatic Cancer

Shivam Saxena, Ankit Gandhi, Pei-Wen Lim, Daniel Relles, Konrad Sarosiek, Christopher Kang, Galina Chipitsyna, Jocelyn Sendecki, Charles J Yeo and Hwyda A Arafat*
Departments of Surgery, Jefferson Pancreatic, Biliary and Related Cancer Center, Thomas Jefferson University, Philadelphia, USA
Corresponding Author : Hwyda A Arafat
Department of Surgery Thomas Jefferson
University 1015 Walnut Street
Suite 618 Curtis Philadelphia
PA 19107, USA
Tel: 215 955-6383
E-mail: [email protected]
Received April 19, 2013; Accepted May 08, 2013; Published May 10, 2013
Citation: Saxena S, Gandhi A, Lim PW, Relles D, Sarosiek K, et al. (2013) RAN GTPase and Osteopontin in Pancreatic Cancer. Pancreatic Dis Ther 3:113. doi:10.4172/2165-7092.1000113
Copyright: © 2013 Saxena S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
 

Abstract

Introduction: Pancreatic ductal adenocarcinoma (PDA) has the worst prognosis among cancers, mainly due to the high incidence of early metastases. RAN small GTPase (RAN) is a protein that plays physiological roles in the regulation of nuclear transport and microtubule spindle assembly. RAN was recently shown to mediate the invasive functions of the prometastatic protein osteopontin (OPN) in breast cancer cells. We and others have shown previously that high levels of OPN are present in PDA. In this study, we analyzed the expression and correlation of RAN with OPN in human pancreatic lesions, and explored their regulation in PDA cell lines. Methods: Real time PCR was used to analyze RAN and OPN mRNA levels in PDA, adjacent non-malignant, and benign pancreatic tissues. Expression levels were correlated with survival and different clinicopathological parameters using different statistical methods. Transient transfection studies using OPN and RAN plasmids, and knockdown experiments using siRNA were used to examine their mutual regulation. Results: OPN and RAN levels highly correlated with each other (p<0.0001). OPN or RAN levels did not correlate with venous lymphatic invasion, diabetes, obesity, T stage, BMI, or survival. However, we found a significant association between RAN levels and perineural invasion (HR=0.79, 95% CI 0.59, 1.07; p=0.0378.). OPN and RAN colocalized in PDA tissues and cell lines. Increasing RAN expression in PDA cells induced OPN transcription and RAN silencing reduced total OPN levels. OPN did not have any significant effect on RAN transcription. Conclusions: The high levels of RAN in PDA and its correlation with OPN and with perineural invasion suggest that RAN may contribute to PDA metastasis and progression through the induction of OPN. RAN’s role in the regulation of OPN in PDA is unique and could provide potential novel therapeutic strategies to combat PDA aggressiveness.

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