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Ocoxin Oral Solution Exerts an Antitumoral Effect in Pancreatic Cancer and Reduces the Stromal-Mediated Chemoresistance

Hernandez-Unzueta, Iera, MS*; Benedicto, Aitor, PhD*; Romayor, Irene, MS*; Herrero, Alba, MS*; Sanz, Eduardo, PhD; Arteta, Beatriz, PhD*; Olaso, Elvira, PhD*; Márquez, Joana, PhD*

doi: 10.1097/MPA.0000000000001277
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Objectives Pancreatic carcinoma is one of the most aggressive cancers overcoming chemoresistance. Thus, novel compounds to complement the current antitumor agents are in need. Ocoxin oral solution (OOS) has proven antioxidant, anti-inflammatory, and antistromagenic properties. The aim of this study was to analyze the effect of OOS in an experimental pancreatic cancer model and its implication in stroma-related chemoresistance to paclitaxel and gemcitabine.

Methods Murine pancreatic carcinoma 266-6 cells were treated with OOS to analyze cell cycle and to perform a mRNA comparative microarray study. Then the viability was assessed in combination with paclitaxel and/or gemcitabine. Chemoresistance induced by the medium taken from fibroblast cultures was also investigated on 6 human pancreatic carcinoma cell lines. Furthermore, an experimental model of pancreatic cancer was carried out to study the effect of OOS in vivo.

Results Ocoxin oral solution enhances the cytotoxic effect of paclitaxel and gemcitabine, while it ameliorates the chemoresistance induced by fibroblast-derived soluble factors in human pancreatic cancer cells. The OOS also promotes the regulation of the expression of genes that are altered in pancreatic carcinoma and slows down 266-6 cell pancreatic tumor development in vivo.

Conclusions Ocoxin oral solution could be a potential complement to the chemotherapeutic drugs for pancreatic adenocarcinoma.

This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

From the *Department of Cellular Biology and Histology, School of Medicine and Dentistry, University of the Basque Country, Leioa; and

Catalysis S.L., Toledo, Spain.

Received for publication July 19, 2018; accepted February 18, 2019.

Address correspondence to: Joana Márquez, PhD, Department of Cell Biology and Histology, University of the Basque Country, Faculty of Medicine and Nursery, Leioa, Barrio sarriena s/n 48940 Leioa, Spain (e-mail: Joana.marquez@ehu.es).

This study was financed by the company Catalysis S.L.

I.H.-U. and A.B. share co–first authorship.

The authors declare no conflict of interest.

Supplemental digital contents are available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s Web site (www.pancreasjournal.com).

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