Background: Gastric cancer is one of the most incident types of cancer worldwide and presents high mortality rates and poor prognosis. oncogene overexpression is a key event in gastric carcinogenesis and it is known that its protein positively regulates CDC25B expression which, in turn, plays an essential role in the cell division cycle progression. Menadione is a synthetic form of vitamin K that acts as a specific inhibitor of the CDC25 family of phosphatases.

Methods: To better understand the menadione mechanism of action in gastric cancer, we evaluated its molecular and cellular effects in cell lines and in , nonhuman primates from the new world which had gastric carcinogenesis induced by N-Methyl-N-nitrosourea. We tested CDC25B expression by western blot and RT-qPCR. assays include proliferation, migration, invasion and flow cytometry to analyze cell cycle arrest. In experiments, in addition to the expression analyses, we followed the preneoplastic lesions and the tumor progression by ultrasonography, endoscopy, biopsies, histopathology and immunohistochemistry.

Results: Our tests demonstrated menadione reducing CDC25B expression and . It was able to reduce migration, invasion and proliferation rates, and induce cell cycle arrest in gastric cancer cell lines. Moreover, our experiments demonstrated menadione inhibiting tumor development and progression.

Conclusions: We suggest this compound may be an important ally of chemotherapeutics in the treatment of gastric cancer. In addition, CDC25B has proven to be an effective target for investigation and development of new therapeutic strategies for this malignancy.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8981514PMC
http://dx.doi.org/10.1177/1756284819895435DOI Listing

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