[Corrigendum] Influence of doxorubicin on apoptosis and oxidative stress in breast cancer cell lines.

IF 7.3 3区 医学 Q1 ONCOLOGY
International journal of oncology Pub Date : 2026-10-01 Epub Date: 2026-07-24 DOI:10.3892/ijo.2026.5923
Nesstor Pilco-Ferreto, Gloria M Calaf
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引用次数: 0

Abstract

Subsequently to the publication of the above article, an interested reader drew to the authors' attention that, concerning the three breast cancer cell lines investigated in their study, it was surprising that they should have detected caspase‑3 expression in the MCF‑7 cell line, as reported for example in Fig. 6, since it has been shown that MCF‑7 cells do not express caspase‑3 (see the paper by Reiner U. Jänicke and colleagues entitled 'MCF‑7 breast carcinoma cells do not express caspase‑3'. Breast Cancer Res Treat vol. 117.1 (2009); p. 219‑221). In their response, the authors acknowledge that the prevailing consensus in the literature, established by the seminal work of Jänicke et al in an article they published in 1998 in Journal of Biological Chemistry holds that MCF‑7 cells harbor a 47‑bp deletion in exon 3 of the CASP3 gene, resulting in a frameshift mutation and a premature stop codon, with consequent absence of detectable functional protein. The authors' own article acknowledged this controversy by citing conflicting reports (references 13 and 39 compared with references 41‑43); however, they also recognize in retrospect that this should have prompted a more circumspect interpretation of their own data. Following a critical re‑evaluation of their methodology, the authors wish to draw attention to the following limitations of the present work: (1) The band detected in MCF‑7 cells using antibody H‑277 cannot be unambiguously attributed to caspase‑3, and cross‑reactivity with co‑expressed proteins of similar molecular weight, most notably caspase‑7, cannot be excluded. (2) The DDRT‑PCR amplicon obtained from MCF‑7 cells with the reported primers may correspond to the aberrant CASP3 transcript arising from the exon 3 deletion, and does not necessarily represent a translation‑competent mRNA. Sequencing of this amplicon was not performed, and would be required to resolve this question. (3) The conclusions of the article on caspase‑3 expression in MCF‑7 cells should therefore be read with these methodological caveats in mind. Importantly, these limitations do not affect the principal findings of the study concerning MDA‑MB‑231 and MCF‑10F cell lines, for which the experimental evidence remains methodologically sound.  The authors are grateful to the Editorial Board of International Journal of Oncology for the rigor of the review process, and also for the opportunity to address these concerns transparently. They also thank the reader of the article for drawing these concerns to their attention. [International Journal of Oncology 49: 753‑762, 2016; DOI: 10.3892/ijo.2016.3558].

[勘误]阿霉素对乳腺癌细胞系凋亡和氧化应激的影响。
在上述文章发表后,一位感兴趣的读者引起了作者的注意,关于他们研究的三种乳腺癌细胞系,令人惊讶的是,他们应该在MCF - 7细胞系中检测到caspase - 3的表达,如图6所示,因为已经表明MCF - 7细胞不表达caspase - 3(见Reiner U. Jänicke及其同事题为“MCF - 7乳腺癌细胞不表达caspase - 3”的论文。乳腺癌Res治疗vol. 117.1 (2009);219 - 221页)。在他们的回应中,作者承认,由Jänicke等人在1998年发表在《生物化学杂志》上的一篇开创性的文章中建立的文献中的普遍共识认为,MCF - 7细胞在CASP3基因的外显子3上含有47 - bp的缺失,导致移码突变和过早停止密码子,从而导致可检测功能蛋白的缺失。作者自己的文章通过引用相互矛盾的报告承认了这一争议(参考文献13和39与参考文献41 - 43相比);然而,回顾过去,他们也认识到,这应该促使他们对自己的数据做出更谨慎的解释。在对他们的方法进行了批判性的重新评估之后,作者希望提请注意当前工作的以下局限性:(1)使用抗体H - 277在MCF - 7细胞中检测到的条带不能明确地归因于caspase - 3,并且不能排除与类似分子量的共表达蛋白(最明显的是caspase - 7)的交叉反应性。(2)用报道的引物从MCF - 7细胞中获得的DDRT - PCR扩增子可能对应于由外显子3缺失引起的异常CASP3转录物,并不一定代表翻译能力强的mRNA。该扩增子的测序没有进行,需要解决这个问题。(3)因此,在阅读这篇关于MCF - 7细胞中caspase - 3表达的文章的结论时,应考虑到这些方法学上的注意事项。重要的是,这些限制并不影响MDA - MB - 231和MCF - 10F细胞系研究的主要结果,实验证据在方法学上仍然是合理的。作者感谢《国际肿瘤学杂志》的编辑委员会严格的审查过程,并有机会透明地解决这些问题。他们也感谢这篇文章的读者提请他们注意这些问题。国际肿瘤学杂志49:753 - 762,2016;DOI: 10.3892 / ijo.2016.3558]。
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
CiteScore
9.60
自引率
0.00%
发文量
157
审稿时长
2.1 months
期刊介绍: The main aim of Spandidos Publications is to facilitate scientific communication in a clear, concise and objective manner, while striving to provide prompt publication of original works of high quality. The journals largely concentrate on molecular and experimental medicine, oncology, clinical and experimental cancer treatment and biomedical research. All journals published by Spandidos Publications Ltd. maintain the highest standards of quality, and the members of their Editorial Boards are world-renowned scientists.
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