Correction to “LncRNA LIMp27 Regulates the DNA Damage Response Through p27 in p53-Defective Cancer Cells”

IF 14.1 1区 材料科学 Q1 CHEMISTRY, MULTIDISCIPLINARY
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引用次数: 0

Abstract

La T, Chen S, Zhao XH, Zhou S, Xu R, Teng L, Zhang YY, Ye K, Xu L, Guo T, Jamaluddin MF, Feng YC, Tang HJ, Wang Y, Xu Q, Gu Y, Cao H, Liu T, Thorne RF, Shao FM, Zhang XD, Jin L. LncRNA LIMp27 Regulates the DNA Damage Response through p27 in p53-Defective Cancer Cells. Adv Sci, 2023 Jan 13; e2204599.

Figure 2i. The images of HT-29.shCtrl untreated (-Dox), treated with Dox (+Dox), Dox withdrawal, HT-29.shLIMp27-1 untreated (-Dox), and HT-29.shLIMp27-2 untreated (-Dox) were incorrect and replaced. The corrected data still demonstrate that Dox treatment inhibits cell clonogenicity associated with reduced LIMp27 expression. Moreover, the recovery of LIMp27 expression after Dox withdrawal partially restores cell clonogenicity, consistent with the conclusion.

Figure 6c. The images of HT-29 control siRNA, HT-29 control siRNA plus Oxaliplatin, HT-29 LIMp27 siRNA-1, WiDr control siRNA, WiDr control siRNA plus Oxaliplatin, WiDr control siRNA plus IR, and WiDr LIMp27 siRNA-1 were incorrect and replaced. The corrected figure does not alter the previous conclusion, namely that LIMp27 knockdown, in combination with oxaliplatin or IR treatment, significantly further reduces cell clonogenicity.

Figure 6g. The images of HT-29 LIMp27 siRNA-1 plus IR, HT-29 LIMp27 siRNA-1 plus p27 siRNA-1 plus Oxaliplatin, and WiDr LIMp27 siRNA-1 plus IR were incorrect and replaced. The corrected figure still demonstrates that the knockdown of p27 diminishes the cooperative effect of LIMp27 knockdown and oxaliplatin or IR treatment in inhibiting the viability of HT-29 and WiDr cells. The conclusion remains unaffected.

Figure s2f. The images of MDA-MB-231 LIMp27 siRNA-1, MCF-7 Control siRNA, MCF-7 LIMp27 siRNA-1, and MCF-7 LIMp27 siRNA-2 were incorrect and replaced. The corrected data still support the original finding that siRNA-mediated LIMp27 knockdown markedly reduces the viability and clonogenicity in mutant p53-expressing cells (MDA-MB-231 and H226), but not in wild-type p53-expressing cells (MCF-7 and A549). The conclusion resmains unaffected.

Figure s4g. The images of HT29 control siRNA, HT29 LIMp27 siRNA-1, HT29 LIMp27 siRNA-1 plus p21 siRNA-1, WiDr control siRNA, WiDr LIMp27 siRNA-1, and WiDr LIMp27 siRNA-1 plus p21 siRNA-1 were incorrect and replaced. The corrected figure corroborates the conclusion that p21 does not mitigate the reductions in clonogenicity.

Figure s8k. The images of HT29 shCtrl treated with Saline only (-Dox) and HT29 shCtrl treated with Saline plus Dox (+Dox) were incorrect and replaced. As the negative control, the corrected images confirm that Dox-induced control shRNA, in combination with saline (vehicle control), does not affect the Ki67-positive cell proportions. Nonetheless, the corrected whole figure upholds the original conclusion that the Dox-induced shRNA knockdown of LIMp27, either alone or in combination with oxaliplatin, leads to a decrease in Ki67-positive cell proportions.

This correction does not affect the overall findings and conclusions of this paper. We apologize for these errors.

更正“LncRNA LIMp27通过p53缺陷癌细胞中的p27调节DNA损伤反应”。
拉婷,陈松,赵小红,周松,徐锐,滕亮,张玉玉,叶凯,徐磊,郭涛,Jamaluddin MF,冯玉春,唐海军,王勇,徐强,顾勇,曹华,刘涛,索恩荣,邵调峰,张晓东,金玲。LncRNA LIMp27通过p27调控p53缺陷癌细胞的DNA损伤反应。科学通报,2013年1月13日;e2204599。图2。HT-29的图像。shCtrl未治疗(-Dox), Dox治疗(+Dox), Dox戒断,HT-29。shLIMp27-1未处理(-Dox)和HT-29。未经处理的shLIMp27-2 (-Dox)不正确并进行更换。校正后的数据仍然表明,Dox处理抑制了与LIMp27表达降低相关的细胞克隆性。此外,停药后LIMp27表达的恢复部分恢复了细胞的克隆原性,与结论一致。图6 c。HT-29对照siRNA、HT-29对照siRNA加奥沙利铂、HT-29 LIMp27 siRNA-1、WiDr对照siRNA、WiDr对照siRNA加奥沙利铂、WiDr对照siRNA加IR、WiDr LIMp27 siRNA-1的图像不正确并进行替换。修正后的数字并没有改变先前的结论,即LIMp27敲低与奥沙利铂或IR治疗联合,可进一步显著降低细胞克隆原性。图6 g。HT-29 LIMp27 siRNA-1加IR、HT-29 LIMp27 siRNA-1加p27 siRNA-1加奥沙利铂、WiDr LIMp27 siRNA-1加IR的图像不正确并被替换。修正后的图仍然表明,p27的敲低降低了LIMp27敲低与奥沙利铂或IR治疗在抑制HT-29和WiDr细胞活力方面的协同作用。结论不受影响。图s2f。MDA-MB-231 LIMp27 siRNA-1、MCF-7 Control siRNA、MCF-7 LIMp27 siRNA-1和MCF-7 LIMp27 siRNA-2的图像不正确,需要替换。修正后的数据仍然支持最初的发现,即sirna介导的LIMp27敲低显著降低了p53表达突变细胞(MDA-MB-231和H226)的活力和克隆性,但在野生型p53表达细胞(MCF-7和A549)中没有这种影响。结论不受影响。图s4g。HT29对照siRNA、HT29 LIMp27 siRNA-1、HT29 LIMp27 siRNA-1 + p21 siRNA-1、WiDr对照siRNA、WiDr LIMp27 siRNA-1、WiDr LIMp27 siRNA-1 + p21 siRNA-1的图像不正确,需要替换。修正后的数字证实了p21不能减轻克隆原性降低的结论。图s8k。单纯盐水(-Dox)处理的HT29 shCtrl和盐水加Dox (+Dox)处理的HT29 shCtrl图像不正确并被替换。作为阴性对照,校正后的图像证实,dox诱导的对照shRNA与生理盐水(对照)联合使用不会影响ki67阳性细胞的比例。尽管如此,校正后的整体数据支持最初的结论,即dox诱导的shRNA敲低LIMp27,无论是单独还是与奥沙利铂联合,都会导致ki67阳性细胞比例的降低。这一修正不影响本文的总体发现和结论。我们为这些错误道歉。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Advanced Science
Advanced Science CHEMISTRY, MULTIDISCIPLINARYNANOSCIENCE &-NANOSCIENCE & NANOTECHNOLOGY
CiteScore
18.90
自引率
2.60%
发文量
1602
审稿时长
1.9 months
期刊介绍: Advanced Science is a prestigious open access journal that focuses on interdisciplinary research in materials science, physics, chemistry, medical and life sciences, and engineering. The journal aims to promote cutting-edge research by employing a rigorous and impartial review process. It is committed to presenting research articles with the highest quality production standards, ensuring maximum accessibility of top scientific findings. With its vibrant and innovative publication platform, Advanced Science seeks to revolutionize the dissemination and organization of scientific knowledge.
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