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Diet, Microbiota, and Colorectal Cancer.饮食、微生物群与结直肠癌
iScience. 2019 Nov 22;21:168-187. doi: 10.1016/j.isci.2019.10.011. Epub 2019 Oct 10.
2
Colorectal cancer.结直肠癌。
Lancet. 2019 Oct 19;394(10207):1467-1480. doi: 10.1016/S0140-6736(19)32319-0.
3
Global burden of colorectal cancer: emerging trends, risk factors and prevention strategies.全球结直肠癌负担：趋势、风险因素和预防策略。
Nat Rev Gastroenterol Hepatol. 2019 Dec;16(12):713-732. doi: 10.1038/s41575-019-0189-8. Epub 2019 Aug 27.
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Post-transcriptional Regulation of Colorectal Cancer: A Focus on RNA-Binding Proteins.结直肠癌的转录后调控：聚焦于RNA结合蛋白
Front Mol Biosci. 2019 Aug 7;6:65. doi: 10.3389/fmolb.2019.00065. eCollection 2019.
5
Increased IGF2BP3 expression promotes the aggressive phenotypes of colorectal cancer cells in vitro and vivo.IGF2BP3 表达增加促进结直肠癌细胞在体外和体内的侵袭表型。
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MiR-494 acts as a tumor promoter by targeting CASP2 in non-small cell lung cancer.miR-494 通过靶向 CASP2 在非小细胞肺癌中发挥肿瘤促进作用。
Sci Rep. 2019 Feb 28;9(1):3008. doi: 10.1038/s41598-019-39453-2.
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Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries.全球癌症统计数据 2018：GLOBOCAN 对全球 185 个国家/地区 36 种癌症的发病率和死亡率的估计。
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The UbL-UBA Ubiquilin4 protein functions as a tumor suppressor in gastric cancer by p53-dependent and p53-independent regulation of p21.UbL-UBA 泛素连接酶 4 蛋白通过依赖 p53 和不依赖 p53 的方式调控 p21，从而发挥抑癌作用，抑制胃癌进展。
Cell Death Differ. 2019 Mar;26(3):516-530. doi: 10.1038/s41418-018-0141-4. Epub 2018 Jun 13.
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RNA Binding Proteins in Intestinal Epithelial Biology and Colorectal Cancer.RNA 结合蛋白在肠道上皮生物学和结直肠癌中的作用。
Trends Mol Med. 2018 May;24(5):490-506. doi: 10.1016/j.molmed.2018.03.008. Epub 2018 Apr 5.
10
Recognition of RNA N-methyladenosine by IGF2BP proteins enhances mRNA stability and translation.IGF2BP 蛋白对 RNA N6-甲基腺苷的识别增强了 mRNA 的稳定性和翻译。
Nat Cell Biol. 2018 Mar;20(3):285-295. doi: 10.1038/s41556-018-0045-z. Epub 2018 Feb 23.

IGF2BP3/ELAVL1复合物对致癌转录本的稳定作用促进结直肠癌的致瘤性。

Stabilization of oncogenic transcripts by the IGF2BP3/ELAVL1 complex promotes tumorigenicity in colorectal cancer.

作者信息

Li Kexin, Huang Furong, Li Yan, Li Dongdong, Lin Hong, Ni Ruoxuan, Zhang Qiao, Zhao Mei, Huang Shengkai, Zou Liang, Huang Changzhi

机构信息

Department of Etiology and Carcinogenesis, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College Beijing 100021, China.

State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College Beijing 100021, China.

出版信息

Am J Cancer Res. 2020 Aug 1;10(8):2480-2494. eCollection 2020.

PMID:32905413
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7471344/
Abstract

The expression of RNA-binding proteins (RBPs) is dysregulated in colorectal cancer (CRC) and in other types of cancer. Among the RBPs, the insulin-like growth factor-2 messenger RNA binding protein (IGF2BP1-3) family is involved in the development of the colon and the progression of CRC. However, the regulation of mRNA fate by IGF2BP3 in CRC remains less well understood. Here, we show that IGF2BP3 interacts with ELAVL1 to coregulate a cohort of genes involved in the cell cycle and cell proliferation. Mechanistically, recognition of these mRNAs by the IGF2BP3/ELAVL1 complex leads to prolonged half-lives of the mRNA molecules and increased expression of the target genes, thereby driving CRC cell proliferation. Interestingly, knockdown of either IGF2BP3 or ELAVL1 impairs the IGF2BP3/ELAVL1 complex-enhanced mRNA stability, suggesting a functional interdependency between IGF2BP3 and ELAVL1 in CRC. Our findings reveal the molecular mechanism by which IGF2BP3 regulates mRNA stability and identify the cooperativity of the IGF2BP3/ELAVL1 complex as a novel therapeutic target in CRC.

摘要

RNA结合蛋白（RBPs）的表达在结直肠癌（CRC）及其他类型癌症中失调。在这些RBPs中，胰岛素样生长因子2信使核糖核酸结合蛋白（IGF2BP1 - 3）家族参与结肠发育及CRC进展。然而，IGF2BP3在CRC中对信使核糖核酸命运的调控仍了解较少。在此，我们表明IGF2BP3与ELAVL1相互作用，共同调控一组参与细胞周期和细胞增殖的基因。从机制上讲，IGF2BP3/ELAVL1复合物对这些信使核糖核酸的识别导致信使核糖核酸分子半衰期延长及靶基因表达增加，从而驱动CRC细胞增殖。有趣的是，敲低IGF2BP3或ELAVL1会损害IGF2BP3/ELAVL1复合物增强的信使核糖核酸稳定性，表明在CRC中IGF2BP3与ELAVL1之间存在功能相互依赖性。我们的研究结果揭示了IGF2BP3调节信使核糖核酸稳定性的分子机制，并确定IGF2BP3/ELAVL1复合物的协同作用是CRC中的一个新治疗靶点。