An Overview of Targeting Legumain for Inhibiting Cancers

(E-pub Ahead of Print)

Author(s): Bandi Deepa Reddy, Bandi Deepa Reddy, Narasimha M Beeraka, Narasimha M Beeraka, CH. M. Kumari Chitturi, CH. M. Kumari Chitturi, SubbaRao V. Madhunapantula*, SubbaRao V. Madhunapantula*

Journal Name: Current Pharmaceutical Design

Become EABM
Become Reviewer
Call for Editor


Legumain (LGMN; EC:, an asparaginyl endopeptidase (AEP) or asparaginyl carboxypeptidase (ACP), is a member of the C13 family of cysteine proteases. Elevated expression of LGMN is reported not only in the tumor cells of breast, prostate and liver but also in the macrophages of the tumor micro-environment. Hence, LGMN is considered as a key protein involved in the regulation of tumor angiogenesis, invasion and metastasis. Targeting LGMN using siRNA or pharmacological agents and peptides was reported to reduce cancer cells proliferation in vitro and shrink tumor size in vivo. Moreover, expression of LGMN is significantly lower in normal cells compared to tumor cells or tumor associated macrophages (TAMs), hence, legumain can be used as a marker for tumor recognition and targeting. Therefore, approaches inhibiting LGMN expression or activity are more viable, less toxic and help in developing the targeted therapeutics. However, to date, LGMN targeting strategies have not been well reported. In this review, an attempt was made to summarize articles pertaining to LGMN (a) structure and activity; (b) oncogenic nature; (c) pharmacological inhibitors; and (d) targeting approaches that inhibit tumor growth. Furthermore, a list of existing gaps in LGMN research is highlighted, which needs additional studies.

Keywords: Legumain, Cancers, TAMs, Metastasis, Targeted therapies, DNA vaccines, miRNAs

Rights & PermissionsPrintExport Cite as

Article Details

(E-pub Ahead of Print)
DOI: 10.2174/1381612826666201125111625
Price: $95

Article Metrics

PDF: 137