On pages 2295 and 2300 in the 15 March 2007 issue, there are errors in Figure 1 and Figure 7. In Figure 1F, the images labeled as control and thalidomide were erroneously duplicated images of overlapping fields of the same original image. The appropriate independent images from the control and thalidomide conditions are now shown in the corrected Figure 1. The images for control and resveratrol-treated cells in Figures 1E and 1F were from the same experiment; therefore, the same images are shown in both panels. The corrected Figure 1 is shown below.
Resveratrol suppresses the proliferation of drug-resistant MM cell lines and potentiates the apoptotic effect of bortezomib and thalidomide. (A-D) U266 cells (5 × 103/100 μL; A), dexamethasone-sensitive (B, left) and dexamethasone-resistant (B, right) MM.1 cells (20 × 103/100 μL), doxorubicin-sensitive (C, left) and doxorubicin-resistant (C, right) RPMI 8266 cells (20 × 103/100 μL), and melphalan-sensitive (D, left) and melphalan-resistant (D, right) RPMI 8266 cells were plated in triplicate, treated with 50 μM resveratrol, and then subjected to MTT assay on days 2, 4, or 6 to analyze proliferation of cells. ○ represents control and ● represents resveratrol-treated cells. Each point on line is an average of triplicate value. Resveratrol induced inhibition of cell growth at days 2 and 4 was statistically significant (P < .05). (E-F) U266 cells (1 × 106/mL) were treated with 25 μM resveratrol and 20 nM bortezomib (E) or 10 μg/mL thalidomide (F) alone or in combination for 24 hours at 37°C. Cells were stained with a live/dead assay reagent for 30 minutes and then analyzed under a fluorescence microscope as described in “Materials and methods.” Percentage of apoptosis is indicated in the inset. (G) U266 cells (1 × 106/mL) were treated with 25 μM resveratrol, 20 nM bortezomib (left), or 10 μg/mL thalidomide (right) alone or in combination for 24 hours at 37°C. Cells were incubated with anti-annexin V antibody conjugated with FITC and then analyzed with a flow cytometer for early apoptotic effects. The results shown are representative of 3 independent experiments. *Values significantly (P < .05) different from control as well as single agent. Error bars represent SD of triplicate values.
Resveratrol suppresses the proliferation of drug-resistant MM cell lines and potentiates the apoptotic effect of bortezomib and thalidomide. (A-D) U266 cells (5 × 103/100 μL; A), dexamethasone-sensitive (B, left) and dexamethasone-resistant (B, right) MM.1 cells (20 × 103/100 μL), doxorubicin-sensitive (C, left) and doxorubicin-resistant (C, right) RPMI 8266 cells (20 × 103/100 μL), and melphalan-sensitive (D, left) and melphalan-resistant (D, right) RPMI 8266 cells were plated in triplicate, treated with 50 μM resveratrol, and then subjected to MTT assay on days 2, 4, or 6 to analyze proliferation of cells. ○ represents control and ● represents resveratrol-treated cells. Each point on line is an average of triplicate value. Resveratrol induced inhibition of cell growth at days 2 and 4 was statistically significant (P < .05). (E-F) U266 cells (1 × 106/mL) were treated with 25 μM resveratrol and 20 nM bortezomib (E) or 10 μg/mL thalidomide (F) alone or in combination for 24 hours at 37°C. Cells were stained with a live/dead assay reagent for 30 minutes and then analyzed under a fluorescence microscope as described in “Materials and methods.” Percentage of apoptosis is indicated in the inset. (G) U266 cells (1 × 106/mL) were treated with 25 μM resveratrol, 20 nM bortezomib (left), or 10 μg/mL thalidomide (right) alone or in combination for 24 hours at 37°C. Cells were incubated with anti-annexin V antibody conjugated with FITC and then analyzed with a flow cytometer for early apoptotic effects. The results shown are representative of 3 independent experiments. *Values significantly (P < .05) different from control as well as single agent. Error bars represent SD of triplicate values.
Resveratrol inhibits the proliferation of CD138+ cells from patients with MM and down-regulates NF-κB and STAT3 activation. (A) Enriched CD138+cells (2 × 105 /0.1 mL) from bone marrow aspirates of patients with multiple myeloma were cultured in the absence or presence of indicated concentrations of resveratrol for 24 hours, and cell proliferation was measured by MTT assay as described in “Materials and methods.” Values represent the mean ± SD of triplicate cultures. *P < .05. (B) Enriched CD138+ cells (2 × 106 cells) from bone marrow aspirates of patients with MM as indicated were cultured in the absence or presence of resveratrol (50 μM) for 12 hours and then tested for NF-κB activity in the nuclei by electrophoretic mobility shift assay as described in “Materials and methods.” (C) STAT3 activation status was determined by fixing the untreated and 12-hour resveratrol-treated (50 μM, 100 μM) enriched CD138+ cells (2 × 106 cells) on slides by cytospin followed by immunocytochemistry for STAT3 as described in “Materials and methods.” Patients’ numbers are indicated beside each panel. Original magnification × 200. One hundred cells were counted for each patient. Grading was as follows: + indicates less than10% cells with nuclear positivity; ++, 10% to 50% cells with nuclear positivity; +++, greater than 51% cells with nuclear positivity. The ++ and + indicate significantly different nuclear (P < .05) positivity than untreated cells. (D) CD138+ cells (2 × 104 cells) from patients no. 8 and no. 9 were treated with 25 μM resveratrol, 20 nM bortezomib, 10 μg/mL thalidomide either alone or in combination for 24 hours at 37°C. Cells were incubated with anti-annexin V antibody conjugated with FITC and then analyzed by a flow cytometer for early apoptotic effects.
Resveratrol inhibits the proliferation of CD138+ cells from patients with MM and down-regulates NF-κB and STAT3 activation. (A) Enriched CD138+cells (2 × 105 /0.1 mL) from bone marrow aspirates of patients with multiple myeloma were cultured in the absence or presence of indicated concentrations of resveratrol for 24 hours, and cell proliferation was measured by MTT assay as described in “Materials and methods.” Values represent the mean ± SD of triplicate cultures. *P < .05. (B) Enriched CD138+ cells (2 × 106 cells) from bone marrow aspirates of patients with MM as indicated were cultured in the absence or presence of resveratrol (50 μM) for 12 hours and then tested for NF-κB activity in the nuclei by electrophoretic mobility shift assay as described in “Materials and methods.” (C) STAT3 activation status was determined by fixing the untreated and 12-hour resveratrol-treated (50 μM, 100 μM) enriched CD138+ cells (2 × 106 cells) on slides by cytospin followed by immunocytochemistry for STAT3 as described in “Materials and methods.” Patients’ numbers are indicated beside each panel. Original magnification × 200. One hundred cells were counted for each patient. Grading was as follows: + indicates less than10% cells with nuclear positivity; ++, 10% to 50% cells with nuclear positivity; +++, greater than 51% cells with nuclear positivity. The ++ and + indicate significantly different nuclear (P < .05) positivity than untreated cells. (D) CD138+ cells (2 × 104 cells) from patients no. 8 and no. 9 were treated with 25 μM resveratrol, 20 nM bortezomib, 10 μg/mL thalidomide either alone or in combination for 24 hours at 37°C. Cells were incubated with anti-annexin V antibody conjugated with FITC and then analyzed by a flow cytometer for early apoptotic effects.
