Loss of phosphatase and tensin homolog enhances cell invasion and migration through aKT/Sp‐1 transcription factor/matrix metalloproteinase 2 activation in hepatocellular carcinoma and has clinicopathologic significance
Karen Man‐Fong Sze, Kris Lai‐Ting Wong, Glanice Kin‐Yan Chu, Joyce Man‐Fong Lee, Tai‐On Yau, Irene Oi‐Lin Ng – 11 February 2011 – Phosphatase and tensin homolog (PTEN) is frequently inactivated in cancers and is associated with advanced stages of cancers or metastasis. However, the molecular mechanism of PTEN in hepatocellular carcinoma (HCC) metastasis is unclear. In this study, we found frequent (47.5%, n = 40) protein underexpression of PTEN in human HCCs compared with their corresponding nontumorous livers.