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Correction to Cells 2021, 10(5), 987.
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Correction

Correction: Sumarni et al. Targeting Cutaneous T-Cell Lymphoma Cells by Ingenol Mebutate (PEP005) Correlates with PKCδ Activation, ROS Induction as Well as Downregulation of XIAP and c-FLIP. Cells 2021, 10, 987

Apoptosis Regulation in Skin Cancer, Skin Cancer Center Charité, Department of Dermatology Venerology und Allergology, Charité—Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany
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Author to whom correspondence should be addressed.
Cells 2025, 14(7), 535; https://doi.org/10.3390/cells14070535
Submission received: 18 December 2024 / Accepted: 21 January 2025 / Published: 3 April 2025
In the original publication [1], there was a mistake in Figure 6 as published. The GAPDH panels in Figures 5f and 6b,f were the same due to the accidental swapping of the blots. The corrected Figure 6 appears below. The authors state that the scientific conclusions are unaffected. This correction was approved by the Academic Editor. The original publication has also been updated.

Reference

  1. Sumarni, U.; Reidel, U.; Eberle, J. Targeting Cutaneous T-Cell Lymphoma Cells by Ingenol Mebutate (PEP005) Correlates with PKCδ Activation, ROS Induction as Well as Downregulation of XIAP and c-FLIP. Cells 2021, 10, 987. [Google Scholar] [CrossRef]
Figure 6. Role of PKCδ in PEP005-induced apoptosis. (a) Effects of PEP005 (50 nM, 24 h) on PKCδ proform (78 kDa) were investigated in four CTCL cell lines. (b,c) Lacking effects of QVD-Oph (QVD, 5 µM, (b)) and vitamin E (VitE, 1 mM, (c)) on PEP005-induced downregulation of PKCδ proform are shown (50 nM, 24 h). (d,e) Inhibition of PEP005-induced apoptosis (d) and restoration of cell viability (e) by Bis-1 in HH and HuT-78. Cells were treated for 24 h with PEP005 (50 nM) and/or Bis-1 (HH, 1 µM; HuT-78, 0.25 µM). (f) Inhibition of PEP005-mediated caspase-3, -8, and -9 processing through Bis-1, as investigated by Western blotting in HH and HuT-78. Cells were treated for 24 h with 50 nM PEP005; Bis-1 was used at 1 (HH) and 0.25 µM (HuT-78), respectively). (g,h) Antagonistic effects of Bis-1 on PEP005-mediated loss of MMP (g) and on PEP005-induced ROS production (h) in cell line HuT-78 (Time: 24 h; PEP005: 50 nM; Bis-1: 0.25 µM). (ac,f) For Western blotting, 30 µg of each protein extract was loaded per lane, and blots were probed with antibodies for PKCδ proform (78 kDa), cleaved caspase-3 (21, 19, 17 kDa), caspase-8 (proform, 57 kDa; cleavage products, 43/41 kDa) and caspase-9 (cleavage product, 35 kDa). GAPDH (37 kDa) was used as loading control. For Western blots, two independent series of protein extracts revealed highly comparable results. (d,e,g,h) Mean values of triplicates ± SDs of representative experiments are shown. At least two independent experiments showed highly comparable results. Statistical significance was calculated from all values (at least 6) and is indicated for combination-treated cells vs. PEP005-treated cells (* p < 0.05).
Figure 6. Role of PKCδ in PEP005-induced apoptosis. (a) Effects of PEP005 (50 nM, 24 h) on PKCδ proform (78 kDa) were investigated in four CTCL cell lines. (b,c) Lacking effects of QVD-Oph (QVD, 5 µM, (b)) and vitamin E (VitE, 1 mM, (c)) on PEP005-induced downregulation of PKCδ proform are shown (50 nM, 24 h). (d,e) Inhibition of PEP005-induced apoptosis (d) and restoration of cell viability (e) by Bis-1 in HH and HuT-78. Cells were treated for 24 h with PEP005 (50 nM) and/or Bis-1 (HH, 1 µM; HuT-78, 0.25 µM). (f) Inhibition of PEP005-mediated caspase-3, -8, and -9 processing through Bis-1, as investigated by Western blotting in HH and HuT-78. Cells were treated for 24 h with 50 nM PEP005; Bis-1 was used at 1 (HH) and 0.25 µM (HuT-78), respectively). (g,h) Antagonistic effects of Bis-1 on PEP005-mediated loss of MMP (g) and on PEP005-induced ROS production (h) in cell line HuT-78 (Time: 24 h; PEP005: 50 nM; Bis-1: 0.25 µM). (ac,f) For Western blotting, 30 µg of each protein extract was loaded per lane, and blots were probed with antibodies for PKCδ proform (78 kDa), cleaved caspase-3 (21, 19, 17 kDa), caspase-8 (proform, 57 kDa; cleavage products, 43/41 kDa) and caspase-9 (cleavage product, 35 kDa). GAPDH (37 kDa) was used as loading control. For Western blots, two independent series of protein extracts revealed highly comparable results. (d,e,g,h) Mean values of triplicates ± SDs of representative experiments are shown. At least two independent experiments showed highly comparable results. Statistical significance was calculated from all values (at least 6) and is indicated for combination-treated cells vs. PEP005-treated cells (* p < 0.05).
Cells 14 00535 g006
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MDPI and ACS Style

Sumarni, U.; Reidel, U.; Eberle, J. Correction: Sumarni et al. Targeting Cutaneous T-Cell Lymphoma Cells by Ingenol Mebutate (PEP005) Correlates with PKCδ Activation, ROS Induction as Well as Downregulation of XIAP and c-FLIP. Cells 2021, 10, 987. Cells 2025, 14, 535. https://doi.org/10.3390/cells14070535

AMA Style

Sumarni U, Reidel U, Eberle J. Correction: Sumarni et al. Targeting Cutaneous T-Cell Lymphoma Cells by Ingenol Mebutate (PEP005) Correlates with PKCδ Activation, ROS Induction as Well as Downregulation of XIAP and c-FLIP. Cells 2021, 10, 987. Cells. 2025; 14(7):535. https://doi.org/10.3390/cells14070535

Chicago/Turabian Style

Sumarni, Uly, Ulrich Reidel, and Jürgen Eberle. 2025. "Correction: Sumarni et al. Targeting Cutaneous T-Cell Lymphoma Cells by Ingenol Mebutate (PEP005) Correlates with PKCδ Activation, ROS Induction as Well as Downregulation of XIAP and c-FLIP. Cells 2021, 10, 987" Cells 14, no. 7: 535. https://doi.org/10.3390/cells14070535

APA Style

Sumarni, U., Reidel, U., & Eberle, J. (2025). Correction: Sumarni et al. Targeting Cutaneous T-Cell Lymphoma Cells by Ingenol Mebutate (PEP005) Correlates with PKCδ Activation, ROS Induction as Well as Downregulation of XIAP and c-FLIP. Cells 2021, 10, 987. Cells, 14(7), 535. https://doi.org/10.3390/cells14070535

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