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Correction: MELK is an oncogenic kinase essential for mitotic progression in basal-like breast cancer cells.

作者信息

Wang Yubao, Li Young-Mi, Baitsch Lukas, Huang Alan, Xiang Yi, Tong Haoxuan, Lako Ana, Von Thanh, Choi Christine, Lim Elgene, Min Junxia, Li Li, Stegmeier Frank, Schlegel Robert, Eck Michael J, Gray Nathanael S, Mitchison Timothy J, Zhao Jean J

出版信息

Elife. 2018 Mar 12;7:e36414. doi: 10.7554/eLife.36414.

DOI:10.7554/eLife.36414
PMID:29528283
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5847332/
Abstract
摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae6b/5847332/5779e7ec0fca/elife-36414-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae6b/5847332/5779e7ec0fca/elife-36414-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae6b/5847332/5779e7ec0fca/elife-36414-fig1.jpg

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Correction: MELK is an oncogenic kinase essential for mitotic progression in basal-like breast cancer cells.更正：MELK是一种致癌激酶，对基底样乳腺癌细胞的有丝分裂进程至关重要。
Elife. 2018 Mar 12;7:e36414. doi: 10.7554/eLife.36414.
2
MELK is not necessary for the proliferation of basal-like breast cancer cells.MELK 对于基底样乳腺癌细胞的增殖并非必需。
Elife. 2017 Sep 19;6:e26693. doi: 10.7554/eLife.26693.
3
MELK expression in ovarian cancer correlates with poor outcome and its inhibition by OTSSP167 abrogates proliferation and viability of ovarian cancer cells.在卵巢癌中，MELK 的表达与不良预后相关，其抑制物 OTSSP167 可消除卵巢癌细胞的增殖和活力。
Gynecol Oncol. 2017 Apr;145(1):159-166. doi: 10.1016/j.ygyno.2017.02.016. Epub 2017 Feb 14.
4
Correction: MELK is an oncogenic kinase essential for metastasis, mitotic progression, and programmed death in lung carcinoma.更正：MELK是一种致癌激酶，对肺癌的转移、有丝分裂进程和程序性死亡至关重要。
Signal Transduct Target Ther. 2024 Jul 13;9(1):186. doi: 10.1038/s41392-024-01910-4.
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MELK-T1, a small-molecule inhibitor of protein kinase MELK, decreases DNA-damage tolerance in proliferating cancer cells.MELK-T1是一种蛋白激酶MELK的小分子抑制剂，可降低增殖癌细胞对DNA损伤的耐受性。
Biosci Rep. 2015 Oct 2;35(6):e00267. doi: 10.1042/BSR20150194.
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MELK expression correlates with tumor mitotic activity but is not required for cancer growth.MELK 表达与肿瘤有丝分裂活性相关，但对肿瘤生长并非必需。
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Involvement of maternal embryonic leucine zipper kinase (MELK) in mammary carcinogenesis through interaction with Bcl-G, a pro-apoptotic member of the Bcl-2 family.母源胚胎亮氨酸拉链激酶（MELK）通过与Bcl-2家族的促凋亡成员Bcl-G相互作用参与乳腺癌发生。
Breast Cancer Res. 2007;9(1):R17. doi: 10.1186/bcr1650.
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Mitotic MELK-eIF4B signaling controls protein synthesis and tumor cell survival.有丝分裂期的MELK-eIF4B信号传导控制蛋白质合成和肿瘤细胞存活。
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CRISPR/Cas9 mutagenesis invalidates a putative cancer dependency targeted in on-going clinical trials.CRISPR/Cas9诱变使正在进行的临床试验中靶向的一种假定的癌症依赖性失效。
Elife. 2017 Mar 24;6:e24179. doi: 10.7554/eLife.24179.
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EZH2 protects glioma stem cells from radiation-induced cell death in a MELK/FOXM1-dependent manner.EZH2 通过依赖于 MELK/FOXM1 的方式保护神经胶质瘤干细胞免受辐射诱导的细胞死亡。
Stem Cell Reports. 2015 Feb 10;4(2):226-38. doi: 10.1016/j.stemcr.2014.12.006. Epub 2015 Jan 15.

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Spatiotemporal regulation of MELK during mitosis.有丝分裂期间MELK的时空调控。
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Differential Effects of Overexpression of Wild Type and Kinase-Dead MELK in Fibroblasts and Keratinocytes, Potential Implications for Skin Wound Healing and Cancer.野生型和激酶失活型 MELK 在成纤维细胞和角质细胞中的差异表达及其对皮肤创伤愈合和癌症的潜在影响。
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本文引用的文献

1
MELK expression correlates with tumor mitotic activity but is not required for cancer growth.MELK 表达与肿瘤有丝分裂活性相关，但对肿瘤生长并非必需。
Elife. 2018 Feb 8;7:e32838. doi: 10.7554/eLife.32838.
2
MELK Promotes Melanoma Growth by Stimulating the NF-κB Pathway.MELK 通过激活 NF-κB 通路促进黑色素瘤生长。
Cell Rep. 2017 Dec 5;21(10):2829-2841. doi: 10.1016/j.celrep.2017.11.033.
3
MELK is not necessary for the proliferation of basal-like breast cancer cells.MELK 对于基底样乳腺癌细胞的增殖并非必需。
通过生物信息学分析鉴定帕金森病的枢纽基因
Front Neurosci. 2022 Nov 8;16:974838. doi: 10.3389/fnins.2022.974838. eCollection 2022.
4
Up-regulation of MELK by E2F1 promotes the proliferation in cervical cancer cells.E2F1 通过上调 MELK 促进宫颈癌细胞的增殖。
Int J Biol Sci. 2021 Sep 7;17(14):3875-3888. doi: 10.7150/ijbs.62517. eCollection 2021.
5
Improving target assessment in biomedical research: the GOT-IT recommendations.提高生物医学研究中目标评估的质量：GOT-IT 建议。
Nat Rev Drug Discov. 2021 Jan;20(1):64-81. doi: 10.1038/s41573-020-0087-3. Epub 2020 Nov 16.
6
Mutant P53 induces MELK expression by release of wild-type P53-dependent suppression of FOXM1.突变型P53通过解除野生型P53对FOXM1的依赖性抑制作用来诱导MELK表达。
NPJ Breast Cancer. 2020 Jan 3;6:2. doi: 10.1038/s41523-019-0143-5. eCollection 2020.
7
A Conditional Dependency on MELK for the Proliferation of Triple-Negative Breast Cancer Cells.三阴性乳腺癌细胞增殖对MELK的条件性依赖。
iScience. 2018 Nov 30;9:149-160. doi: 10.1016/j.isci.2018.10.015. Epub 2018 Oct 18.
Elife. 2017 Sep 19;6:e26693. doi: 10.7554/eLife.26693.
4
CRISPR/Cas9 mutagenesis invalidates a putative cancer dependency targeted in on-going clinical trials.CRISPR/Cas9诱变使正在进行的临床试验中靶向的一种假定的癌症依赖性失效。
Elife. 2017 Mar 24;6:e24179. doi: 10.7554/eLife.24179.
5
Toward the Validation of Maternal Embryonic Leucine Zipper Kinase: Discovery, Optimization of Highly Potent and Selective Inhibitors, and Preliminary Biology Insight.迈向母体胚胎亮氨酸拉链激酶的验证：发现、高效和选择性抑制剂的优化以及初步生物学见解
J Med Chem. 2016 May 26;59(10):4711-23. doi: 10.1021/acs.jmedchem.6b00052. Epub 2016 May 17.
6
MELK is an oncogenic kinase essential for mitotic progression in basal-like breast cancer cells.MELK是一种致癌激酶，对基底样乳腺癌细胞的有丝分裂进程至关重要。
Elife. 2014 May 20;3:e01763. doi: 10.7554/eLife.01763.