Focal Adhesion Kinase as a Therapeutic Target of Bortezomib

ISSN: 1875-5992 (Online)
ISSN: 1871-5206 (Print)

Volume 17, 14 Issues, 2017

Download PDF Flyer

Anti-Cancer Agents in Medicinal Chemistry

Formerly: Current Medicinal Chemistry - Anti-Cancer Agents

This journal supports open access

Aims & ScopeAbstracted/Indexed in

Ranking and Category:
  • 27th of 59 in Chemistry, Medicinal

Submit Abstracts Online Submit Manuscripts Online

Michelle Prudhomme
Institut de Chimie de Clermont-Ferrand
Université Clermont Auvergne

View Full Editorial Board

Subscribe Purchase Articles Order Reprints

Current: 2.722
5 - Year: 2.849

Focal Adhesion Kinase as a Therapeutic Target of Bortezomib

Anti-Cancer Agents in Medicinal Chemistry, 10(10): 747-752.

Author(s): Bor-Sheng Ko, Tzu-Ching Chang and Jun-Yang Liou.

Affiliation: Institute of Cellular and System Medicine, National Health Research Institutes, 35 Keyan Road, Zhunan, Miaoli County 35053, Taiwan.


Bortezomib, a modified dipeptidyl boronic acid, is a selective potent proteasome inhibitor that has been approved for clinical treatment of multiple myeloma and mantel cell lymphoma. Results from a growing number of basic studies and clinical trials reveal that bortezomib could be used to treat diverse types of solid tumors alone or in combination with other chemotherapeutic drugs. It has been shown that bortezomib transcriptionally suppresses focal adhesion kinase (FAK) expression by interrupting the nuclear factor kappa B (NFκB) pathway, which suggests that FAK could be a potential molecular target for bortezomib. Analysis of FAK promoter sequences revealed that FAK promoter harbors the NFκB and p53 binding domains. Further studies of FAK promoter activity, real-time PCR, electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) assay revealed that bortezomib inhibits NFκB binding on the FAK promoter, thereby reducing FAK expression. Thus, bortezomib could inhibit cancer cell growth and migration or invasion by repressing FAK expression. Since activation and overexpression of FAK has been implicated in the progression and invasion of malignant tumors, it is likely that targeting FAK with bortezomib is a potential strategy for preventing cancer metastasis. This review focuses on the molecular regulation of FAK and the potential clinical application of bortezomib.


Bortezomib, Focal adhesion kinase, NFκB, p53, proteasome inhibitor, cancer treatment, Hepatocellular carcinoma, hematological malignancies, chromatin immunoprecipitation, EMSA, boronic acid, ubiquitin-proteasome, TRAIL, epoxomycin, actacystin.

Purchase Online Order Reprints Order Eprints Rights and Permissions

Article Details

Volume: 10
Issue Number: 10
First Page: 747
Last Page: 752
Page Count: 6
DOI: 10.2174/187152010794728666
Price: $58
Global Biotechnology Congress 2017Drug Discovery and Therapy World Congress 2017

Related Journals

Related eBooks

Webmaster Contact: Copyright © 2017 Bentham Science