Fig. 2.
Fig. 2. Coadministration of bryostatin 1 overcomes the protective effects of Bcl-2 against paclitaxel-induced apoptosis. / (A) U937/neo (■), U937/Bcl-2 (░), and U937/ΔBcl-2 (▪) cells were treated with paclitaxel (Tax; 10 nM) with or without bryostatin 1 (Bry; 10 nM) for 24 hours. Apoptotic cells were quantified by annexin V and PI positivity as described in “Materials and methods.” (B) Cells were treated as in panel A, after which they were washed free of drug and plated in soft agar, after which colonies consisting of at least 50 cells were scored after 12 days. Values were expressed as a percentage relative to untreated controls (Con). Values for panels A and B represent the means ± SE for 3 separate experiments involving different U937/Bcl-2 and U937/ΔBcl-2 clones. *Significant difference compared with treatment with paclitaxel or bryostatin 1 alone (P < .001).

Coadministration of bryostatin 1 overcomes the protective effects of Bcl-2 against paclitaxel-induced apoptosis.

(A) U937/neo (■), U937/Bcl-2 (░), and U937/ΔBcl-2 (▪) cells were treated with paclitaxel (Tax; 10 nM) with or without bryostatin 1 (Bry; 10 nM) for 24 hours. Apoptotic cells were quantified by annexin V and PI positivity as described in “Materials and methods.” (B) Cells were treated as in panel A, after which they were washed free of drug and plated in soft agar, after which colonies consisting of at least 50 cells were scored after 12 days. Values were expressed as a percentage relative to untreated controls (Con). Values for panels A and B represent the means ± SE for 3 separate experiments involving different U937/Bcl-2 and U937/ΔBcl-2 clones. *Significant difference compared with treatment with paclitaxel or bryostatin 1 alone (P < .001).

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