Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Annexin A1 and leukemia: A systematic review

Ernieda Hatah¹, Phylicia Gan Yin Hui², Endang Kumolosasi²

¹Centre of Quality Management of Medicines; ²Drug and Herbal Research Centre, Faculty of Pharmacy, Universiti Kebangsaan Malaysia, Kuala Lumpur, Malaysia.

For correspondence:- Endang Kumolosasi Email: e_kumolosasi@ukm.edu.my Tel:+60392898054

Accepted: 17 November 2019 Published: 31 December 2019

Citation: Hatah E, Hui PG, Kumolosasi E. Annexin A1 and leukemia: A systematic review. Trop J Pharm Res 2019; 18(12):2653-2668 doi: 10.4314/tjpr.v18i12.26

© 2019 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To review systematically the involvement of Annexin A1 (ANXA1) in various leukemia cells in order to advance the understanding of ANXA1 role in leukemia.

Methods: The systematic review was carried out via a comprehensive search of electronic databases for all relevant articles published up to September 2017. Specific key words were used to retrieve the articles. All articles were imported into EndNote software while duplicates were removed from the list. The retrieved articles were selected using inclusion and exclusion criteria.

Results: FK228, a novel HDACi and FR235222, increased expression of ANXA1 in Kasumi-1, SKNO-1 and U937 cells, respectively, and induced apoptosis. The study also neutralized ANXA1 in the same cells, which caused a complete blockage of the FK228-induced apoptosis. Resveratrol was reported to markedly increase ANXA1 levels which led to caspase 3-mediated apoptosis on HL-60 cells. Dexamethasone, 17β-estradiol (E2β), all-trans retinoic acid and okadaic acid enhanced ANXA1 mRNA expression in U937, human CCRF-CEM, ATRA-NB4 and HL-60 cell lines. Rp-8-Br-cAMPs prevented dexamethasone-, E2β- and dBcAMP-induced ANXA1 synthesis via the activation of cAMP-respond-element binding protein (CREB). ANXA1 levels were reduced dramatically in K562/ADR cells as compared to K562 cells. When ANXA1 was upregulated by transfection in these cells, the cells exhibited a decrease in resistance to ADR and vincristine.

Conclusion: ANXA1 expression is induced by different drugs which leads to apoptosis in different types of cell. ANXA1 plays a role in the drug resistance of leukemic cells.

Keywords: Annexin A1, ANXA1, Lipocortin-1, Renocortin, Leukemia