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Volume 14
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Correction

Correction: Di Crosta et al. Valemetostat–SAHA-Driven Acetylation of p53 via SET/TAF-Iβ Displacement and p300 Activation Modulates Cell Cycle Regulators in Pancreatic Cancer Cells. Biomedicines 2025, 13, 2279

by
Michele Di Crosta
1,
Francesca Chiara Ragone
1,
Rossella Benedetti
1,
Gabriella D’Orazi
2,3,
Roberta Santarelli
1,
Maria Saveria Gilardini Montani
1,* and
Mara Cirone
1,*
1
Department of Experimental Medicine, Sapienza University of Rome, 00161 Rome, Italy
2
Faculty of Medicine, UniCamillus—Saint Camillus International University of Health and Medical Sciences, 00131 Rome, Italy
3
Unit of Cellular Networks and Molecular Therapeutic Targets, IRCCS Regina Elena National Cancer Institute, 00144 Rome, Italy
*
Authors to whom correspondence should be addressed.
Biomedicines 2026, 14(5), 1159; https://doi.org/10.3390/biomedicines14051159
Submission received: 15 April 2026 / Accepted: 11 May 2026 / Published: 20 May 2026
(This article belongs to the Section Cell Biology and Pathology)
Browse Figure
Versions Notes
In the original publication [1], there was a mistake in Figure 5 as published.
The mistake consists of the overlap between the lane corresponding to Lamin b for PT45 cells in Figure 5B and the lane corresponding to GADPH (p21) for PT45 cells in Figure 4A, taken from a previously published paper by the same authors [2].
The corrected Figure 5 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.

References

  1. Di Crosta, M.; Ragone, F.C.; Benedetti, R.; D’Orazi, G.; Santarelli, R.; Gilardini Montani, M.S.; Cirone, M. Valemetostat–SAHA-Driven Acetylation of p53 via SET/TAF-Iβ Displacement and p300 Activation Modulates Cell Cycle Regulators in Pancreatic Cancer Cells. Biomedicines 2025, 13, 2279. [Google Scholar] [CrossRef] [PubMed]
  2. Di Crosta, M.; Ragone, F.C.; Benedetti, R.; D’Orazi, G.; Gilardini Montani, M.S.; Cirone, M. SAHA/5-AZA Enhances Acetylation and Degradation of mutp53, Upregulates p21 and Downregulates c-Myc and BRCA-1 in Pancreatic Cancer Cells. Int. J. Mol. Sci. 2024, 25, 7020. [Google Scholar] [CrossRef] [PubMed]
Biomedicines 14 01159 g005
Figure 5. SAHA/DS, particularly with 5-AZA supplementation, reduces pancreatic cancer cell survival, downregulates CHK1, and increases DNA damage in pancreatic cancer cells. (A) Cell survival as evaluated by Trypan blue exclusion assay in PaCa44 and PT45 cell lines, untreated (CT) or treated with SAHA, SAHA/DS, or DS. The histograms indicate the percentage of cell viability relative to the control; data are shown as the mean plus SD from more than three experiments. * p-value < 0.05; ** p < 0.01 and **** p < 0.0001 as calculated by ANOVA test. In addition, the synergistic cytotoxicity induced by combination treatment, as evaluated by the Bliss independence model, is reported (Bliss index > 1). (B) Cleaved Caspase 3 (cl Casp3) expression level as investigated by Western blotting in PaCa44 and PT45 cells undergoing the above-reported treatments. Lamin b was used as the loading control. Histograms are the mean plus SD of the densitometric analysis carried out in three experiments, expressing the ratio between cleaved Caspase3 and lamin b; * p-value < 0.05 and **** p < 0.0001 as calculated by ANOVA test. (C) Representative pictures of PaCa44 cell colonies following staining with crystal violet and histograms representing the quantitative analyses of colony formation shown as mean ± SD of percent on untreated cells (CT). (D) γH2AX and CHK1 expression as evaluated by Western blotting analysis in PaCa44 cells untreated (CT) or treated by SAHA, SAHA/DS, and DS. GAPDH represented the loading control. (E) FACS profiles of Paca44 cells treated as reported above. The numbers indicate the percentage of subG1 events. One experiment out of three is shown. (F) p21, CHK1, and γH2AX expression as evaluated by Western blotting in PaCa44 cells pre-treated (+) or not (−) with pifithrin-α and exposed to SAHA/DS or left untreated (CT). GAPDH was the loading control. (G) p21, CHK1, and γH2AX expression as evaluated by Western blotting in PaCa44 cells untreated (CT) or treated by SAHA/DS in the presence or absence of 5-AZA. GAPDH was the loading control. (H) Cell survival as evaluated by Trypan blue exclusion assay in PaCa44 cell lines treated by SAHA/DS in the presence or absence of 5-AZA or left untreated. Histograms represent the mean plus SD of the densitometric analysis derived from three experiments and expressed as the ratio between (B) cl Casp3/lamin b, (D) γH2AX/GAPDH and CHK1/GAPDH, (F) p21/GAPDH, CHK1/GAPDH, and γH2AX/GAPDH, and (G) p21/GAPDH and γH2AX/GAPDH. * p-value < 0.05; ** p < 0.01; *** p < 0.001; and **** p < 0.0001 as calculated by ANOVA test.
Figure 5. SAHA/DS, particularly with 5-AZA supplementation, reduces pancreatic cancer cell survival, downregulates CHK1, and increases DNA damage in pancreatic cancer cells. (A) Cell survival as evaluated by Trypan blue exclusion assay in PaCa44 and PT45 cell lines, untreated (CT) or treated with SAHA, SAHA/DS, or DS. The histograms indicate the percentage of cell viability relative to the control; data are shown as the mean plus SD from more than three experiments. * p-value < 0.05; ** p < 0.01 and **** p < 0.0001 as calculated by ANOVA test. In addition, the synergistic cytotoxicity induced by combination treatment, as evaluated by the Bliss independence model, is reported (Bliss index > 1). (B) Cleaved Caspase 3 (cl Casp3) expression level as investigated by Western blotting in PaCa44 and PT45 cells undergoing the above-reported treatments. Lamin b was used as the loading control. Histograms are the mean plus SD of the densitometric analysis carried out in three experiments, expressing the ratio between cleaved Caspase3 and lamin b; * p-value < 0.05 and **** p < 0.0001 as calculated by ANOVA test. (C) Representative pictures of PaCa44 cell colonies following staining with crystal violet and histograms representing the quantitative analyses of colony formation shown as mean ± SD of percent on untreated cells (CT). (D) γH2AX and CHK1 expression as evaluated by Western blotting analysis in PaCa44 cells untreated (CT) or treated by SAHA, SAHA/DS, and DS. GAPDH represented the loading control. (E) FACS profiles of Paca44 cells treated as reported above. The numbers indicate the percentage of subG1 events. One experiment out of three is shown. (F) p21, CHK1, and γH2AX expression as evaluated by Western blotting in PaCa44 cells pre-treated (+) or not (−) with pifithrin-α and exposed to SAHA/DS or left untreated (CT). GAPDH was the loading control. (G) p21, CHK1, and γH2AX expression as evaluated by Western blotting in PaCa44 cells untreated (CT) or treated by SAHA/DS in the presence or absence of 5-AZA. GAPDH was the loading control. (H) Cell survival as evaluated by Trypan blue exclusion assay in PaCa44 cell lines treated by SAHA/DS in the presence or absence of 5-AZA or left untreated. Histograms represent the mean plus SD of the densitometric analysis derived from three experiments and expressed as the ratio between (B) cl Casp3/lamin b, (D) γH2AX/GAPDH and CHK1/GAPDH, (F) p21/GAPDH, CHK1/GAPDH, and γH2AX/GAPDH, and (G) p21/GAPDH and γH2AX/GAPDH. * p-value < 0.05; ** p < 0.01; *** p < 0.001; and **** p < 0.0001 as calculated by ANOVA test.
Biomedicines 14 01159 g005
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MDPI and ACS Style

Di Crosta, M.; Ragone, F.C.; Benedetti, R.; D’Orazi, G.; Santarelli, R.; Gilardini Montani, M.S.; Cirone, M. Correction: Di Crosta et al. Valemetostat–SAHA-Driven Acetylation of p53 via SET/TAF-Iβ Displacement and p300 Activation Modulates Cell Cycle Regulators in Pancreatic Cancer Cells. Biomedicines 2025, 13, 2279. Biomedicines 2026, 14, 1159. https://doi.org/10.3390/biomedicines14051159

AMA Style

Di Crosta M, Ragone FC, Benedetti R, D’Orazi G, Santarelli R, Gilardini Montani MS, Cirone M. Correction: Di Crosta et al. Valemetostat–SAHA-Driven Acetylation of p53 via SET/TAF-Iβ Displacement and p300 Activation Modulates Cell Cycle Regulators in Pancreatic Cancer Cells. Biomedicines 2025, 13, 2279. Biomedicines. 2026; 14(5):1159. https://doi.org/10.3390/biomedicines14051159

Chicago/Turabian Style

Di Crosta, Michele, Francesca Chiara Ragone, Rossella Benedetti, Gabriella D’Orazi, Roberta Santarelli, Maria Saveria Gilardini Montani, and Mara Cirone. 2026. "Correction: Di Crosta et al. Valemetostat–SAHA-Driven Acetylation of p53 via SET/TAF-Iβ Displacement and p300 Activation Modulates Cell Cycle Regulators in Pancreatic Cancer Cells. Biomedicines 2025, 13, 2279" Biomedicines 14, no. 5: 1159. https://doi.org/10.3390/biomedicines14051159

APA Style

Di Crosta, M., Ragone, F. C., Benedetti, R., D’Orazi, G., Santarelli, R., Gilardini Montani, M. S., & Cirone, M. (2026). Correction: Di Crosta et al. Valemetostat–SAHA-Driven Acetylation of p53 via SET/TAF-Iβ Displacement and p300 Activation Modulates Cell Cycle Regulators in Pancreatic Cancer Cells. Biomedicines 2025, 13, 2279. Biomedicines, 14(5), 1159. https://doi.org/10.3390/biomedicines14051159

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