Effects of STC1 overexpression on tumorigenicity and metabolism of hepatocellular carcinoma

• DOI: 10.18632/oncotarget.23566
• Publication Date: 2017-12-21T21:21:50Z
• Authors: Cherry CT Leung; Chris KC Wong
• Keywords: Ribosomal protein s6

Stanniocalcin-1 (STC1) is a paracrine factor associated with inflammation and carcinogenesis. Using clinicopathological data, we previously reported that greater expression of STC1 in hepatocellular carcinoma (HCC) was significantly correlated smaller tumor size. The underlying mechanism on the correlation not known. In this study, using metastatic HCC cell-line (MHCC-97L, P) lentiviral vector mediated-STC1 overexpression, inoculation STC1-overexpressing MHCC-97L (S1) cells nude mice xenograft model demonstrated reductions mass volume. As compared P cells, S1 exhibited epithelial phenotype lower plating efficiency reduced migratory proliferative potential. coulter counter for cell-sizing, (17.6 μm) were than (19.6 μm). Western blot analysis revealed level phosphorylated ribosomal protein S6 (p-rpS6). Moreover, an inhibition upstream kinase p70S6K evident dephosphorylation Thr389 linker domain kinase. p70S6K/p-rpS6 pathway accompanied cellular ATP increase p-AMPK cells. Significantly rates glycolysis extracellular O2 consumption energy status. Since faster rate production essential to support cancer growth metastasis, present study identified effect STC1-overexpression reducing metabolism, leading activation AMPK but signaling reduce growth.