癌症专家《Nature》文章出错

生物通报道，近期《Cell》杂志宣布华人学者的一篇发表于2000年的文章因图片出现问题而被撤回（详细报道见：http://www.ebiotrade.com/newsf/2009-2/200926172128.htm），时隔不久，《Nature》杂志也发现免疫学专家2007年Michael Karin发表在Nature上的一篇文章出现类似的情况，不过幸运的是，Karin教授的文章没有遭Nature杂志撤回，而是在最新一期的Nature杂志上（2月12日）刊登勘误信息。

 

Michael Karin教授是美国加州大学圣地亚哥分校药理学系的教授，主要研究肿瘤发生，与肿瘤侵入转移机制。主要的研究课题IKKβ在B淋巴细胞发育，基础细胞生物学，癌症，炎症发生过程中的信号转导机制。据不完全统计，Michael Karin在顶级期刊上发表了不少文章，到目前为止，3篇Nature，2篇Cell，1篇Science，3篇Cancer Cell等。

 

在最新一期的Nature杂志上，勘误文章内容称，在2007年发表的以：Nuclear cytokine-activated IKK controls prostate cancer metastasis by repressing Maspin为题的文章中，Fig.2a (Kai1

and Mkk4 control lanes)中的对照泳道图在图片收集过程中不经意地重复了，其他的对照孔和实验Maspin泳道的结果都是正确的。为慎重起见，研究小组重复了该实验，获得了相同的结论。该论文的原始数据能在补充材料中找到。

 

Nature勘误报道如下：

Corrigendum

Nature 457, 920 (12 February 2009)

Nuclear cytokine-activated IKK controls prostate cancer metastasis by repressing Maspin

Jun-Li Luo, Wei Tan, Jill M. Ricono, Olexandr Korchynskyi, Ming Zhang,

Steven L. Gonias, David A. Cheresh & Michael Karin

 

Nature 446, 690–694 (2007)

It has come to our attention that some of the control lanes in Fig. 2a (Kai1 and Mkk4 control lanes) may have been inadvertently duplicated during figure assembly; the other control lanes and the experimental Maspin lanes are correct. We have therefore repeated the experiments and obtained the same results as those in the published figure. The primary data from this experiment can be found in Supplementary Information.

 

2007年Nature原文检索：

Letter

Nature 446, 690-694 (5 April 2007) | doi:10.1038/nature05656

Nuclear cytokine-activated IKK controls prostate cancer metastasis by repressing Maspin

【Abstract】

Nuclear cytokine-activated IKK controls prostate cancer metastasis by repressing Maspin

Inflammation enhances tumour promotion through NF-B-dependent mechanisms1. NF-B was also proposed to promote metastatogenesis through epithelial–mesenchymal transition2. Yet a mechanistic link between inflammation and metastasis is missing. We identified a role for IB kinase  (IKK), activated by receptor activator of NF-B (RANK/TNFRSF11A), in mammary epithelial proliferation during pregnancy3. Owing to similarities between mammary and prostate epithelia, we examined IKK involvement in prostate cancer and its progression. Here we show that a mutation that prevents IKK activation slows down CaP growth and inhibits metastatogenesis in TRAMP mice, which express SV40 T antigen in the prostate epithelium4. Decreased metastasis correlated with elevated expression of the metastasis suppressor Maspin5, the ablation of which restored metastatic activity. IKK activation by RANK ligand (RANKL/TNFSF11) inhibits Maspin expression in prostate epithelial cells, whereas repression of Maspin transcription requires nuclear translocation of active IKK. The amount of active nuclear IKK in mouse and human prostate cancer correlates with metastatic progression, reduced Maspin expression and infiltration of prostate tumours with RANKL-expressing inflammatory cells. We propose that tumour-infiltrating RANKL-expressing cells lead to nuclear IKK activation and inhibition of Maspin transcription, thereby promoting the metastatic phenotype.