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Published on: May 15, 2019
CDC25B Inhibition by Menadione: A Potential New Therapeutical Approach
Helem Ferreira Ribeiro1, Carla de Castro Sant' Anna2, Valdenira de Jesus Oliveira Kato3
1University Center of Pará, Campus João Paulo do Valle Mendes, Av. Alm. Barroso, 3775, Souza, 66613-903, Belém, Pará, Brazil.
Abstract:
Gastric cancer (GC) is the fifth most common type of tumor and the third leading cause of cancer death worldwide. The evolution of gastric carcinogenesis is still poorly understood and, for this reason, preclinical research protocols were established that included the development of gastric cancer cell lines and the establishment of models of gastric carcinogenesis in non-human primates such as Sapajus apella. A comprehensive literature search was performed in relevant databases such as PubMed, ResearchGate, and Google Scholar to identify studies related to the topic. After an in-depth study of these reports, significant data were collected and compiled under appropriate headings. The main result of the studies carried out by the group on GC is the demonstration of the MYC gene overexpression as a common phenomenon in stomach carcinogenesis. Furthermore, we revealed that reducing the expression of the CDC25B gene, regulated by the MYC protein, is a therapeutic strategy against stomach tumors. This review article reveals preclinical evidence that treatment with menadione in experimental models of gastric tumorigenesis, in vivo and in vitro, inhibits the action of the phosphatase CDC25B and, consequently, prevents cell proliferation, invasion, and migration.
Insights
Gastric cancer research reveals MYC gene overexpression is common. Reducing CDC25B gene expression, regulated by MYC, offers a potential therapeutic strategy for stomach tumors.
Area of Science:
- Oncology
- Molecular Biology
- Preclinical Research
Background:
- Gastric cancer (GC) is a leading cause of cancer death globally.
- The mechanisms of gastric carcinogenesis are not fully understood.
- Preclinical models, including cell lines and non-human primates, are crucial for studying GC.
Purpose of the Study:
- To review preclinical evidence on gastric carcinogenesis.
- To identify key molecular mechanisms in stomach tumor development.
- To explore potential therapeutic strategies for gastric cancer.
Main Methods:
- Comprehensive literature search of PubMed, ResearchGate, and Google Scholar.
- Analysis of studies on gastric cancer cell lines and animal models.
- Compilation and synthesis of data on gastric carcinogenesis.
Main Results:
- MYC gene overexpression is a common finding in stomach carcinogenesis.
- The CDC25B gene, regulated by MYC, plays a role in tumor progression.
- Reducing CDC25B expression is identified as a potential therapeutic target.
Conclusions:
- Menadione treatment in preclinical models inhibits CDC25B phosphatase activity.
- This inhibition prevents cancer cell proliferation, invasion, and migration.
- Targeting CDC25B offers a promising therapeutic avenue for gastric cancer.
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