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. Author manuscript; available in PMC: 2013 Jul 1.

Published in final edited form as: Cancer Lett. 2012 Feb 2;320(1):111–121. doi: 10.1016/j.canlet.2012.01.037

Fig. 3 — Ainp1 suppressed the CoCl₂-activated, HRE-driven luciferase activity in Hep3B cells. A, cells (± 100 μM CoCl₂) were transfected with the same amount of plasmid DNA (EV, pCMV- Tag4A; Ainp1, pCMV-Ainp1; C 553, pCMV-C 553). Amount of plasmid DNA used: +, 0.3 μg; ++, 0.6 μg; 150 ng of pGL3-Epo reporter luciferase plasmid; 50 ng of pCH110 plasmid. This experiment was repeated once with similar results. B, cells (± 100 μM CoCl₂) were transfected with the same amount of plasmid DNA (EV1, pCMV-Tag4A; EV2, pSport; Ainp1, pCMV-Tag4-Ainp1; ARNT, pSport-ARNT). Amount of plasmid DNA used: +, 0.2 μg; ++, 0.4 μg; ++++, 0.8 μg; 75 ng of pGL3-Epo reporter luciferase plasmid; 25 ng of pCH110 plasmid. This experiment was repeated once with similar results. Luciferase activity was normalized by the β-galactosidase activity. Error bars indicate the variations of the means (mean ± SD, n = 3). ***p < 0.001.

Fig. 3 — Ainp1 suppressed the CoCl₂-activated, HRE-driven luciferase activity in Hep3B cells. A, cells (± 100 μM CoCl₂) were transfected with the same amount of plasmid DNA (EV, pCMV- Tag4A; Ainp1, pCMV-Ainp1; C 553, pCMV-C 553). Amount of plasmid DNA used: +, 0.3 μg; ++, 0.6 μg; 150 ng of pGL3-Epo reporter luciferase plasmid; 50 ng of pCH110 plasmid. This experiment was repeated once with similar results. B, cells (± 100 μM CoCl₂) were transfected with the same amount of plasmid DNA (EV1, pCMV-Tag4A; EV2, pSport; Ainp1, pCMV-Tag4-Ainp1; ARNT, pSport-ARNT). Amount of plasmid DNA used: +, 0.2 μg; ++, 0.4 μg; ++++, 0.8 μg; 75 ng of pGL3-Epo reporter luciferase plasmid; 25 ng of pCH110 plasmid. This experiment was repeated once with similar results. Luciferase activity was normalized by the β-galactosidase activity. Error bars indicate the variations of the means (mean ± SD, n = 3). ***p < 0.001.