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. Author manuscript; available in PMC: 2013 Feb 13.
Published in final edited form as: Adv Drug Deliv Rev. 2007 Mar 16;59(2-3):141–152. doi: 10.1016/j.addr.2007.03.008

Figure 5.

Figure 5

Maximum Fluo-4 fluorescence in cultured U87 human glioma cells is shown after stimulation with 200 ng/ml human epidermal growth factor (EGF). Prior to measurement of calcium induced fluorescence, the cells were pre-incubated for 24 hours with either vehicle (A) or HIRMAb-targeted PILs carrying clone 967 plasmid DNA at a dose of 0.5 μg DNA per dish (B). From [37]. (C) U87 human glioma cells were exposed to clone 967, clone 882, clone 952, or clone 962 plasmid DNA for 48 hours and harvested for EGFR Western blotting. Films were scanned and quantified with NIH Image software, arbitrary densitometric units (ADU) were computed for each treatment group. A representative scan is shown at the top of each mean ± SE (n=3–4 dishes). Clone 967 and 952 produces shRNAs against the human EGFR and the luciferase mRNAs, respectively. Clone 882 produces a 700 nt antisense RNA against the human EGFR. Clone 962 encodes a shRNA against the EGFR that produces no knockdown of EGFR expression From [37]. (D, E) Confocal microscopy of intra-cranial glioma. Sections are shown for brain tumors from RNAi treated mice (D) or saline treated mice (E). The sections are doubly labeled with the murine 528 MAb to the EGFR (green) and the rat 8D3 MAb to the mouse TfR (red). There is decreased immunoreactive EGFR in the tumor cells in the RNAi treated mice (D) relative to the saline treated mice (E). From [37].