Taken together, we can conclude that hypoxia induces RECK downregulation through the recruitment of HDAC1 and HIF-1alpha to the rHRE2 site in the promoter and the inhibition of hypoxic RECK silencing would be a therapeutic and preventive target for early tumorigenesis.
The reversion-inducing-cysteine-rich protein with Kazal motifs (RECK) has a significant effect on tumorigenesis by limiting angiogenesis and invasion of tumors through the extracellular matrix.
The RASSF1AAla133Ser polymorphism, RECK gene polymorphism and for the first time haplotype of both genes influence molecular carcinogenesis and clinic pathological features of HCC within the Egyptian population.