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. Author manuscript; available in PMC: 2012 May 1.
Published in final edited form as: Oral Oncol. 2011 Mar 21;47(5):371–375. doi: 10.1016/j.oraloncology.2011.02.018

Figure 1. Direct and Paracrine upregulation of ANGPTL4 by vGPCR.

Figure 1

(A) angptl4 mRNA levels (qRT-PCR), upon transfection of pCEFL AU5 vGPCR (vGPCR) or pCEFL AU5 GFP (Control) in HMEC1. Induction of angptl4 mRNA by hypoxia (1% O2; 24 hr) was used as a control. (B–C) Cellular ANGPTL4 (WB) (B) and secreted ANGPTL4 (ELISA) (C) of HMEC1 transfected with pCEFL Tet REV TA and pBIG AU5 vGPCR (Tet-vGPCR). Cells were left untreated or treated with (1 µg/ml) Dox for 2h or 4h. Induction of ANGPTL4 expression by hypoxia (1% O2; 12hr or 24hr) was used as a control. (D) Representative H&E staining and immunohistochemical detection of (AU5) vGPCR expressing cells as well as ANGPTL4 and VEGF expression in murine vGPCR tumors. (E) Upregulation in HMEC1 of ANGPTL4 upon transfection of pCEFL AU5 vGPCR (vGPCR) or pCEFL AU5 GFP (Control), treatment with conditioned media of vGPCR-expressing cells (vGPCR CM), or exposure to individual recombinant factors present in vGPCR conditioned media.