Next Article in Journal
Possible DNA Viral Factors of Human Breast Cancer
Next Article in Special Issue
Role of Uncoupling Proteins in Cancer
Previous Article in Journal
Molecular Mechanisms of Mouse Skin Tumor Promotion
Previous Article in Special Issue
The Role of Oxidative Stress in Carcinogenesis Induced by Metals and Xenobiotics
Open AccessReview

Nrf2 and NF-κB and Their Concerted Modulation in Cancer Pathogenesis and Progression

Dipartimento Medicina Sperimentale Scienze Biochimiche, Sezione Biochimica Cellulare, Università di Perugia, Via del giochetto, 06124 Perugia, Italy
*
Author to whom correspondence should be addressed.
Cancers 2010, 2(2), 483-497; https://doi.org/10.3390/cancers2020483
Received: 26 February 2010 / Revised: 18 March 2010 / Accepted: 12 April 2010 / Published: 13 April 2010
(This article belongs to the Special Issue Oxidative Stress and Cancer)
Reactive oxygen species, produced by oxidative stress, are implicated in the initiation, promotion, and malignant conversion of carcinogenesis through activation/suppression of redox-sensitive transcription factors. NF-E2-related factor 2 (Nrf2) encodes for antioxidant and general cytoprotection genes, while NF-κB regulates the expression of pro-inflammatory genes. A variety of anti-inflammatory or anti-carcinogenic phyto-chemicals suppress NF-κB signalling and activate the Nrf2-ARE pathway. In this review we consider the role of Nrf2 and NF-κB in cancer pathogenesis and progression, focusing on their concerted modulation and potential cross-talk. View Full-Text
Keywords: oxidative stress; chemoprevention; chemotherapy oxidative stress; chemoprevention; chemotherapy
Show Figures

Graphical abstract

MDPI and ACS Style

Bellezza, I.; Mierla, A.L.; Minelli, A. Nrf2 and NF-κB and Their Concerted Modulation in Cancer Pathogenesis and Progression. Cancers 2010, 2, 483-497.

Show more citation formats Show less citations formats

Article Access Map by Country/Region

1
Only visits after 24 November 2015 are recorded.
Search more from Scilit
 
Search
Back to TopTop