In this article , which was published in the July 2009 issue of Molecular Cancer Therapeutics (1), the authors apologize for errors in which Figs. 3D and 4 were labeled incorrectly.
![Figure 3. Narciclasine induces stress fiber formation in human glioblastoma multiforme cells. A, fluorescence microscopy visualization of the actin cytoskeleton [red fluorescence, globular (nonpolymerized) actin; green fluorescence, fibrillary (polymerized) actin] in control (CT) and narciclasine-treated (100 nmol/L) U373 glioblastoma multiforme cells after 2 hours. B, quantitative determination of the intensity (absorbance) of green fluorescence (polymerized actin) in untreated glioblastoma multiforme cells (CT) versus those treated for 10 minutes (GL19 cells: green columns), 30 minutes (Hs683 cells: blue columns), or 45 minutes (U373 cells, red columns) with 100 nmol/L narciclasine (Narci). One hundred cells were analyzed per cell line and condition. Mean ± SE. P values of statistical significance refer to the comparison (Mann–Whitney U test) between untreated and narciclasine-treated groups. ***, P < 0.001. C, postulated model summarizing the hypothesis of narciclasine-mediated actin stress fiber stabilization. D, determination by means of immunofluorescence (top; GL19 cells) and Western blotting (bottom; Hs683 cells) of the expression of phospho-cofilin (phosphorylated at Ser3) in glioblastoma multiforme cells left untreated (CT) or treated with 100 nmol/L narciclasine after 15 minutes and during a kinetic of treatment from 0 to 180 minutes, respectively.](https://aacr.silverchair-cdn.com/aacr/content_public/journal/mct/11/5/10.1158_1535-7163.mct-12-0327/3/m_1216fig3.jpeg?Expires=1728690882&Signature=XrC9usCGmUcw9Z5pf9USlGrYSIbpR86cs3kGKw2FXgaEZJd2dMxwYgKLFSWQ8gPodzUyf5iXaT2PJDUVsGipuEiJmbLFYlpYhj-cWOiC58AhuSLbL0jV9CyaCxFq3JAyFORPAbfGlDqqi8Sgjlk9ZpNppXhCfxPUZVkXGglBXTbr~cKTbnZqWeKWNfnQi7APzwlTHQUXmfsnfdfyrO5k19VP1tdmjq7jXNmz0JKqoTYjg5ipdQfaozoF0o6GhPjeNiF-g6SIcAluPgoGKwm0Cze35zZe3dIy62msNYSbbBQkfYq0e0DH5TFjCp2lqR1lnlJOJphCAYZrcVqvmXlb0g__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA)
Narciclasine induces stress fiber formation in human glioblastoma multiforme cells. A, fluorescence microscopy visualization of the actin cytoskeleton [red fluorescence, globular (nonpolymerized) actin; green fluorescence, fibrillary (polymerized) actin] in control (CT) and narciclasine-treated (100 nmol/L) U373 glioblastoma multiforme cells after 2 hours. B, quantitative determination of the intensity (absorbance) of green fluorescence (polymerized actin) in untreated glioblastoma multiforme cells (CT) versus those treated for 10 minutes (GL19 cells: green columns), 30 minutes (Hs683 cells: blue columns), or 45 minutes (U373 cells, red columns) with 100 nmol/L narciclasine (Narci). One hundred cells were analyzed per cell line and condition. Mean ± SE. P values of statistical significance refer to the comparison (Mann–Whitney U test) between untreated and narciclasine-treated groups. ***, P < 0.001. C, postulated model summarizing the hypothesis of narciclasine-mediated actin stress fiber stabilization. D, determination by means of immunofluorescence (top; GL19 cells) and Western blotting (bottom; Hs683 cells) of the expression of phospho-cofilin (phosphorylated at Ser3) in glioblastoma multiforme cells left untreated (CT) or treated with 100 nmol/L narciclasine after 15 minutes and during a kinetic of treatment from 0 to 180 minutes, respectively.
Narciclasine induces stress fiber formation in human glioblastoma multiforme cells. A, fluorescence microscopy visualization of the actin cytoskeleton [red fluorescence, globular (nonpolymerized) actin; green fluorescence, fibrillary (polymerized) actin] in control (CT) and narciclasine-treated (100 nmol/L) U373 glioblastoma multiforme cells after 2 hours. B, quantitative determination of the intensity (absorbance) of green fluorescence (polymerized actin) in untreated glioblastoma multiforme cells (CT) versus those treated for 10 minutes (GL19 cells: green columns), 30 minutes (Hs683 cells: blue columns), or 45 minutes (U373 cells, red columns) with 100 nmol/L narciclasine (Narci). One hundred cells were analyzed per cell line and condition. Mean ± SE. P values of statistical significance refer to the comparison (Mann–Whitney U test) between untreated and narciclasine-treated groups. ***, P < 0.001. C, postulated model summarizing the hypothesis of narciclasine-mediated actin stress fiber stabilization. D, determination by means of immunofluorescence (top; GL19 cells) and Western blotting (bottom; Hs683 cells) of the expression of phospho-cofilin (phosphorylated at Ser3) in glioblastoma multiforme cells left untreated (CT) or treated with 100 nmol/L narciclasine after 15 minutes and during a kinetic of treatment from 0 to 180 minutes, respectively.
Involvement of several elements of the RhoA/ROCK/LIMK/cofilin pathway in the antitumor effects of narciclasine. Western blot analysis of the expression of phospho-serine/threonine protein kinases (U373 cells), ROCK1 (U373 cells), and phosphorylated LIMK1/2 (GL19 cells) in glioblastoma multiforme cells left untreated or treated with 100 nmol/L narciclasine (0–180 min). Tub, tubulin.
Involvement of several elements of the RhoA/ROCK/LIMK/cofilin pathway in the antitumor effects of narciclasine. Western blot analysis of the expression of phospho-serine/threonine protein kinases (U373 cells), ROCK1 (U373 cells), and phosphorylated LIMK1/2 (GL19 cells) in glioblastoma multiforme cells left untreated or treated with 100 nmol/L narciclasine (0–180 min). Tub, tubulin.
Figure 3D was initially labeled as “GL19.” In fact, the top of Fig. 3D relates to the GL19 glioma cell line, whereas the bottom of Fig. 3D relates to the Hs683 glioma cell line as indicated in the corrected Fig. 3D.
Figure 4 was initially labeled as “GL19.” In fact, both the top (PPserthreo proteins) and middle (ROCK1) refer to the U373 glioma cell line, whereas the bottom (phospho-LIMK1/2) relates to the GL19 glioma cell line as indicated in the corrected Fig. 4.
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