C-Met inhibitor linked to less cell proliferation, significant apoptosis in metastatic HCC cell line-- Eric Metcalf
Wednesday, September 29, 2010 (Last Updated: 09/29/2010)
WEDNESDAY, Sept. 29 (HealthDay News) -- Targeting c-Met, a receptor for hepatocyte growth factor that plays a role in growth, invasion, and metastasis of liver cancer, may be useful in treating patients with hepatocellular carcinoma (HCC) and c-Met positive tumors, according to research presented at the American Association for Cancer Research International Conference on Molecular Diagnostics in Cancer Therapeutic Development, held from Sept. 27 to 30 in Denver.
Hanning You, M.D., and Carl Barth Rountree, M.D., of the Pennsylvania State University College of Medicine in Hershey, discussed their work using two human HCC cell lines: Huh7 cells, which have no significant metastatic properties, and MHCC97-H cells, which can be highly metastatic.
The researchers found that MHCC97-H had lower expression of E-Cadherin and greater expression of c-Met, fibronectin, and Zeb2 compared to Huh7 cells. The use of the c-Met inhibitor PHA665752 inhibited cell proliferation and colony formation in MHCC97-H cells, and also led to a significant level of apoptosis in MHCC97-H cells compared to Huh7 cells. In a tumor xenograft model of MHCC97-H cells in nude mice, daily use of PHA665752 for 12 days inhibited tumor growth compared to vehicle-treated mice.
"Current therapies for HCC patients are 'one size fits all.' We propose that molecular profiling will enable better therapy for HCC patients with a c-Met positive tumor," You said in a statement.
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