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. Author manuscript; available in PMC: 2014 Jan 6.

Published in final edited form as: Mol Cancer Res. 2009 Nov 10;7(11):10.1158/1541-7786.MCR-09-0255. doi: 10.1158/1541-7786.MCR-09-0255

Cav-1 enhances mRNA stabilities of VEGF, TGF-β1, and FGF2. A. cav-1–manipulated LNTB25cav, DU145, and PC-3 cells were treated with 10 µg/mL of actinomycin in the presence and absence of LY for the indicated times, followed by quantitative RT-PCR analysis for mRNA levels of VEGF, TGF-β1, and FGF2. Error bars indicate SD. The data were fitted with linear trend lines, and the data from actinomycin treatment for 1 and 2 h were subjected to statistical analysis. * is used for the comparison to control (–) doxycycline (doxy) or NC siRNA, and ♦ is used for the comparison of (+) doxy + LY with (+) doxy or NC siRNA+LY with NC siRNA. * or ♦ indicates statistically significant (P < 0.05), and ** or ♦♦ indicates statistically very significant (P < 0.0001). B. diagram summarizes cav-1–GF autoregulatory loop. T = testosterone.

Cav-1 enhances mRNA stabilities of VEGF, TGF-β1, and FGF2. A. cav-1–manipulated LNTB25cav, DU145, and PC-3 cells were treated with 10 µg/mL of actinomycin in the presence and absence of LY for the indicated times, followed by quantitative RT-PCR analysis for mRNA levels of VEGF, TGF-β1, and FGF2. Error bars indicate SD. The data were fitted with linear trend lines, and the data from actinomycin treatment for 1 and 2 h were subjected to statistical analysis. * is used for the comparison to control (–) doxycycline (doxy) or NC siRNA, and ♦ is used for the comparison of (+) doxy + LY with (+) doxy or NC siRNA+LY with NC siRNA. * or ♦ indicates statistically significant (P < 0.05), and ** or ♦♦ indicates statistically very significant (P < 0.0001). B. diagram summarizes cav-1–GF autoregulatory loop. T = testosterone.