Radiation-enhanced hepatocellular carcinoma cell invasion with MMP-9 expression through PI3K/Akt/NF-kappaB signal transduction pathway.
作者： J C-H Cheng , C H Chou , M L Kuo , C-Y Hsieh
关键词: LY294002 、 Cell 、 PI3K/AKT/mTOR pathway 、 Carcinogenesis 、 Biology 、 Wortmannin 、 Endocrinology 、 Cell culture 、 Internal medicine 、 Cancer research 、 Signal transduction 、 Protein kinase B
摘要: This study is to investigate the molecular mechanism of radiation-enhanced cell invasiveness hepatocellular carcinoma (HCC) correlating with clinical patients undergoing radiotherapy and subsequently developing metastasis. Three HCC lines (HepG2, Hep3B Huh7) normal hepatocyte line (CL-48) were irradiated different doses. The effect radiation on was determined using Boyden chamber assay. Radiation-enhanced invasion capability evident in cells but not hepatocytes. Invasion observed gelatin-coated fibronectin-coated or type I collagen-coated membranes. Radiation upregulated matrix metalloproteinase-9 (MMP-9) mRNA level, MMP-9 protein level activity. antisense oligonucleotides inhibited radiation-induced expression thereby significantly invasion. Furthermore, phosphatidylinositol 3-kinase (PI3K)/Akt chemical inhibitors LY294002 wortmannin suppressed expression. Transient transfection dominant-negative Akt plasmid also showed that PI3K/Akt-signaling pathway involved this Moreover, nuclear factor-kappaB (NF-kappaB) decoy oligodeoxynucleotide enhanced promoter activity completely. PI3K/Akt NF-kappaB-driven luciferase Taken together, our results indicated sublethal dose could enhance by through PI3K/Akt/NF-kappaB signal transduction pathway.
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