The aim of this study was to inhibit breast tumor cell proliferation by modulating c-Fos and Fra-1 and regulate membrane biogenesis by controlling lipid synthesis rates.
More importantly, these phosphorylations were required for Fra-1-induced migration of breast cancer cells and phosphorylated Fra-1 expression was enriched at the invasion front of human breast tumors.
This downregulation correlated with an increased expression of the Fra-1 gene, which was reported to act as a pro-oncogene by supporting the invasion and progression of breast tumors.
The FHIT gene is located at the FRA 3B fragile site at chromosome 3p 14.2, and alterations in the FHIT gene and Fhit protein have been found associated with genome instability, particularly in BRCA 2 mutated breast tumours.