Aims Pancreatic ductal adenocarcinoma (PDAC) is one of the most fatal malignancies. Hence, there is a need for new markers and treatment strategies. P68/DEAD box protein 5 (DDX5) is an ATP-dependent RNA helicase of the DEAD box protein family. It is a prognostic marker for several cancers. In this study, we aimed to evaluate the expression and clinical relevance of DDX5 in PDAC.
Methods DDX5 expression in tissue microarray blocks containing 230 PDAC samples was examined using immunohistochemical analysis. DDX5 expression was considered high when more than 50% of the cells were stained and low when less than 50% of the cells were stained. We investigated the association between DDX5 expression and clinicopathological parameters, including patient survival.
Results The nuclei of normal pancreatic ducts, normal acinar cells and PDAC cells were stained positive for DDX5 although the intensity and distribution of DDX5 expression varied. Islet cells showed strong and diffuse staining of DDX5. DDX5 expression was low and high in 148 (64.3%) and 82 cases (35.7%), respectively. Low DDX5 expression was significantly associated with an advanced pT factor (pT2–pT3: tumour size,>20 mm), lymphatic involvement, advanced tumour-node-metastasis (TNM) stage (stages IIB, III, and IV), and venous involvement. In addition, the multivariate analysis revealed that DDX5 expression is an independent prognostic factor for PDAC.
Conclusion These results suggest that DDX5 plays an important role in tumour invasiveness and PDAC prognosis.
- pancreatic neoplasms
Statistics from Altmetric.com
Handling editor Dhirendra Govender.
Contributors MM and KH conceived and designed the study, interpreted immunohistochemical staining results, performed the statistical analyses and wrote the manuscript. MM also performed immunohistochemistry, prepared tissue microarray blocks and summarised clinicopathological data. TS and YU prepared tissue microarray blocks and samples for immunohistochemistry. YT supported the immunohistochemistry analysis and reviewed the manuscript. AK summarised clinicopathological data. NN, HS and TK reviewed the manuscript.
Funding This work was supported by Tokai University School of Medicine Research-Aid Grant 2018 and JSPS KAKENHI (grant number 20K17034).
Competing interests None declared.
Patient consent for publication Not required.
Ethics approval This study was approved by the Clinical Research Committee of Tokai University (approval No. 17R275).
Provenance and peer review Not commissioned; externally peer reviewed.
Data availability statement All data relevant to the study are included in the article.
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.