Replicative Stress and the FHIT Gene: Roles in Tumor Suppression, Genome Stability and Prevention of Carcinogenesis

Cancers

Jenna R. Karras¹  Kay Huebner¹  Carolyn A. Paisie¹ 

[1] Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA;

关键词: oxidative stress;    reactive oxygen species;    common fragile sites;    genome instability;   

DOI  :  10.3390/cancers6021208

来源: DOAJ

【 摘 要 】

The fragile FHIT gene, encompassing the chromosomal fragile site FRA3B,is an early target of DNA damage in precancerous cells. While vulnerable to DNA damage itself, FHIT protein expression is essential to protect from DNA damage-induced cancer initiation and progression by modulating genome stability, oxidative stress and levels of accumulating DNA damage. Thus, FHIT, whose expression is lost or reduced in many human cancers, is a tumor suppressor and genome caretaker whose loss initiates genome instability in preneoplastic lesions. Ongoing studies are seeking more detailed understanding of the role of FHIT in the cellular response to oxidative damage. This review discussesthe relationship between FHIT, reactive oxygen species production, and DNA damage in the context of cancer initiation and progression.

【 授权许可】

Unknown