Structural and Functional Properties of Activator Protein-1 in Cancer and Inflammation

Author:

Bhosale Pritam Bhagwan1ORCID,Kim Hun Hwan1ORCID,Abusaliya Abuyaseer1ORCID,Vetrivel Preethi1ORCID,Ha Sang Eun1ORCID,Park Min Yeong1ORCID,Lee Ho Jeong2ORCID,Kim Gon Sup1ORCID

Affiliation:

1. Research Institute of Life Science and College of Veterinary Medicine, Gyeongsang National University, Gazwa, Jinju 52828, Republic of Korea

2. Biological Resources Research Group, Gyeongnam Department of Environmental Toxicology and Chemistry, Korea Institute of Toxicology, 17 Jegok-gil, Jinju 52834, Republic of Korea

Abstract

The transcriptional machinery is composed of numerous factors that help to regulate gene expression in cells. The function and the fundamental role of transcription factors in different human diseases and cancer have been extensively researched. Activator protein-1 (AP-1) is an inducible transcription factor that consists of a diverse group of members including Jun, Fos, Maf, and ATF. AP-1 involves a number of processes such as proliferation, migration, and survival in cells. Dysfunctional AP-1 activity is seen in several diseases, especially cancer and inflammatory disorders. The AP-1 proteins are controlled by mitogen-activated protein kinases (MAPKs) and the NF-κB pathway. AP-1 inhibitors can be actively pursued as drug discovery targets in cancer therapy when used as a treatment to halt tumor progression. The consumption of phytochemicals in the diet is related to decreasing the incidence of cancer and proves to exhibit anticancer properties. Natural product targets AP-1 are effective cancer prevention and treatment options for various cancer types. Targeting AP-1 with natural products is an effective cancer treatment option for different cancer types. This review summarizes AP-1 subunit proteins, their structures, AP-1-related signaling, and its modulation by natural bioactive compounds.

Funder

National Research Foundation

Publisher

Hindawi Limited

Subject

Complementary and alternative medicine

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