Fig. 8.
Fig. 8. TNF soluble receptor (sTNFR) abrogates bryostatin 1–mediated potentiation of paclitaxel-induced apoptosis. / U937 cells (A) and HL-60 (B) cells were exposed to paclitaxel (5 nM) with or without bryostatin 1 (10 nM) for 24 hours in the presence (▪) and absence (░)of sTNFR (100 ng/mL). Apoptosis was determined by annexin V and PI positivity as described in “Materials and methods.” Values are representative of 3 separate experiments (means ± SE). U937 cells were exposed to the treatments described for panels A and B for 24 hours, after which caspase-8 (C) and caspase-3 (D) activities, reflected by IETD-pNA or DEVD-pNA cleavage, respectively, were determined as described in “Materials and methods.” Values represent percentages relative to untreated controls and correspond to the 3 separate experiments performed in triplicate (means ± SE). *Significant difference from cells exposed to paclitaxel/bryostatin 1 in the absence of sTNFR (P < .01).

TNF soluble receptor (sTNFR) abrogates bryostatin 1–mediated potentiation of paclitaxel-induced apoptosis.

U937 cells (A) and HL-60 (B) cells were exposed to paclitaxel (5 nM) with or without bryostatin 1 (10 nM) for 24 hours in the presence (▪) and absence (░)of sTNFR (100 ng/mL). Apoptosis was determined by annexin V and PI positivity as described in “Materials and methods.” Values are representative of 3 separate experiments (means ± SE). U937 cells were exposed to the treatments described for panels A and B for 24 hours, after which caspase-8 (C) and caspase-3 (D) activities, reflected by IETD-pNA or DEVD-pNA cleavage, respectively, were determined as described in “Materials and methods.” Values represent percentages relative to untreated controls and correspond to the 3 separate experiments performed in triplicate (means ± SE). *Significant difference from cells exposed to paclitaxel/bryostatin 1 in the absence of sTNFR (P < .01).

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