Our previous research showed that loss of Tg737 is associated with hepatoma cell invasion and migration; therefore, we hypothesized that the Tg737 signal might be required for hypoxia-enhanced invasion and migration.
Deletions of the Tg737 gene, whose product is involved in liver oval cell proliferation, differentiation, and ploidy control, have been recently shown in chemically induced rat liver tumors and in a limited series of patients with hepatocellular carcinoma (HCC).
The Tg737 gene was found to be altered in approximately 40% of the rodent chemically-induced liver tumors, 40% of the human liver tumors, and in liver, kidney and pancreatic human tumor cell lines.
Ectopic re-expression of the Tg737 gene in a Tg737 deleted mouse liver tumor cell line resulted in suppression of tumorigenic growth, without altering in vitro cell culture growth.