• Home
  • Search Results
  • Annexin A2 inhibition suppresses ovarian cancer progression via regulating β-catenin/EMT.

Annexin A2 inhibition suppresses ovarian cancer progression via regulating β-catenin/EMT.

Oncology reports (2017-04-26)
Yan Liu, Hongyu Li, Zhenying Ban, Manman Nai, Li Yang, Yannan Chen, Yiming Xu
ABSTRACT

Annexin A2 is a member of the Annexin family that acts as a Ca2+-dependent phospholipid and membrane binding protein, which is associated with the survival and spread of multiple neoplasms. However, the function of Annexin A2 in ovarian cancer progression remains unclear. In this study, we aimed to investigate the role and underlying molecular mechanism of Annexin A2 in cell proliferation and invasion in ovarian cancer. We found that the mRNA expression of Annexin A2 was upregulated in ovarian cancer tissues and cell lines. In the loss-of-function of Annexin A2, β-catenin was indicated to be significantly suppressed and EMT constrained. Moreover, cell proliferation and invasion were both markedly inhibited by the downregulation of Annexin A2. Additionally, the overexpression of β-catenin obviously reversed the effect of Annexin A2 on EMT, and cell proliferation and invasion, indicating that Annexin A2 suppression regulated EMT through controlling β-catenin. Taken together, this study showed that Annexin A2 inhibition suppresses proliferation and invasion in ovarian cancer via β-catenin/EMT, proposing the potential role of Annexin A2 in the prevention and treatment of ovarian cancer.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
MISSION® esiRNA, targeting human ANXA2

Social Media

LinkedIn icon
Twitter icon
Facebook Icon
Instagram Icon

Merck

Research. Development. Production.

We are a leading supplier to the global Life Science industry with solutions and services for research, biotechnology development and production, and pharmaceutical drug therapy development and production.

© 2021 Merck KGaA, Darmstadt, Germany and/or its affiliates. All Rights Reserved.

Reproduction of any materials from the site is strictly forbidden without permission.