Correction to “Discovery of Novel 5-Cyano-3-phenylindole-Based LSD1/HDAC Dual Inhibitors for Colorectal Cancer Treatment”

IF 6.8 1区 医学 Q1 CHEMISTRY, MEDICINAL Journal of Medicinal Chemistry Pub Date : 2025-04-11 DOI:10.1021/acs.jmedchem.5c00900
Hui-Juan Zhu, Hui-Min Zhou, Xiao-Xiao Zhou, Shi-Jie Li, Meng-Jie Zheng, Zhen Xu, Wen-Jing Dai, Yi-Bo Ban, Meng-Yao Zhang, Yi-Zhe Zhang, Jia-Rui Lu, Yong-Tao Xu, Sai-Qi Wang, Xiao-Jing Shi, Ying-Chao Duan
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Abstract

In our study investigating the impact of target compound 20c alongside positive control drugs (ORY-1001 and SAHA) on the expression levels of HDAC and LSD1 substrate proteins─specifically, Ac-tubulin, Ac-H3, Ac-H4, H3K4me1, H3K4me2, and H3K4me3─we conducted a series of experiments on different tumor cell lines, including HCT-116 and HT-29 cells. Regrettably, during the assembly of Figure 7 in the original manuscript, we inadvertently used an incorrect image for H3K4me1 and H3 in Figure 7E. Upon a recent and thorough review of the original manuscript and raw data, we identified this error and have now replaced the incorrect image with the correct one in the revised Figure 7. All authors have agreed to the change. The corrected figure still demonstrates that compound 20c significantly upregulates the expression level of H3K4me1, and this correction do not alter the scientific conclusions of our study in any way. Figure 7. Compound 20c simultaneously inhibited LSD1 and HDAC activities in HCT-116 and HT-29 cells. (A-D) Western blot analysis of the effects of compound 20c on the expression levels of Ac-tubulin, Ac-H3, Ac-H4, and H3 in HCT-116 and HT-29 cells; (E–H) Western blot analysis of the effects of compound 20c on the expression levels of H3K4me1, H3K4me2, H3K4me3, LSD1, and H3 in HCT-116 and HT-29 cells; (I, J) CETSA of LSD1 with 20c at 5.0 μM in HCT-116 and HT-29 lysates for 6 h; (K) CETSA of LSD1 with 20c at different concentrations (1.25, 2.5, and 5.0 μM) in HCT-116 lysates for 6 h; (L) Western blot analysis of the effects of compound 24 on the levels of H3K4me1, H3K4me2, and Ac-H3. We sincerely regret any confusion this may have caused and appreciate the readers’ understanding as we take the necessary steps to ensure the accuracy and integrity of our research. This article has not yet been cited by other publications.

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对 "发现治疗结直肠癌的新型 5-Cyano-3-phenylindole-Based LSD1/HDAC 双抑制剂 "的更正
在我们研究目标化合物20c与阳性对照药物(ry -1001和SAHA)对HDAC和LSD1底物蛋白(特别是ac -微管蛋白、Ac-H3、Ac-H4、H3K4me1、H3K4me2和H3K4me3)表达水平的影响时,我们在不同的肿瘤细胞系(包括HCT-116和HT-29细胞)上进行了一系列实验。很遗憾,在原稿中对图7的组装过程中,我们无意中使用了图7E中H3K4me1和H3的错误图像。在最近对原始手稿和原始数据进行了彻底的检查后,我们发现了这个错误,现在已经用修改后的图7中的正确图像替换了不正确的图像。所有作者都同意这一改变。修正后的数据仍然表明化合物20c显著上调了H3K4me1的表达水平,这一修正并不会改变我们研究的科学结论。图7。化合物20c同时抑制HCT-116和HT-29细胞中LSD1和HDAC的活性。(A-D) Western blot分析化合物20c对HCT-116和HT-29细胞ac -微管蛋白、Ac-H3、Ac-H4、H3表达水平的影响;(E-H) Western blot分析化合物20c对HCT-116、HT-29细胞中H3K4me1、H3K4me2、H3K4me3、LSD1、H3表达水平的影响;(I, J) LSD1在5.0 μM的20c条件下在HCT-116和HT-29裂解物中停留6 h的CETSA;(K)不同浓度(1.25、2.5和5.0 μM) 20c对LSD1在HCT-116裂解物中作用6 h的CETSA;(L) Western blot分析化合物24对H3K4me1、H3K4me2和Ac-H3水平的影响。我们对由此可能造成的任何混乱表示诚挚的歉意,并感谢读者的理解,因为我们采取了必要的措施来确保我们研究的准确性和完整性。这篇文章尚未被其他出版物引用。
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来源期刊
Journal of Medicinal Chemistry
Journal of Medicinal Chemistry 医学-医药化学
CiteScore
4.00
自引率
11.00%
发文量
804
审稿时长
1.9 months
期刊介绍: The Journal of Medicinal Chemistry is a prestigious biweekly peer-reviewed publication that focuses on the multifaceted field of medicinal chemistry. Since its inception in 1959 as the Journal of Medicinal and Pharmaceutical Chemistry, it has evolved to become a cornerstone in the dissemination of research findings related to the design, synthesis, and development of therapeutic agents. The Journal of Medicinal Chemistry is recognized for its significant impact in the scientific community, as evidenced by its 2022 impact factor of 7.3. This metric reflects the journal's influence and the importance of its content in shaping the future of drug discovery and development. The journal serves as a vital resource for chemists, pharmacologists, and other researchers interested in the molecular mechanisms of drug action and the optimization of therapeutic compounds.
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