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Krüppel样因子6剪接变体1:一种参与多种恶性肿瘤进展的致癌转录因子。

Krüppel-Like Factor 6 Splice Variant 1: An Oncogenic Transcription Factor Involved in the Progression of Multiple Malignant Tumors.

作者信息

Hu Kang, Zheng Qing-Kang, Ma Rui-Jie, Ma Chao, Sun Zhi-Gang, Zhang Nan

机构信息

School of Clinical Medicine, Weifang Medical University, Weifang, China.

Cheeloo College of Medicine, Shandong University, Jinan, China.

出版信息

Front Cell Dev Biol. 2021 Mar 18;9:661731. doi: 10.3389/fcell.2021.661731. eCollection 2021.

DOI:10.3389/fcell.2021.661731
PMID:33816511
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8017371/
Abstract

Krüppel-like factor 6 (KLF6) is one of the most studied members of the specificity protein/Krüppel-like factor (SP/KLF) transcription factor family. It has a typical zinc finger structure and plays a pivotal role in regulating the biological processes of cells. Recently, it has been considered to play a role in combatting cancer. Krüppel-like factor 6 splice variant 1 (KLF6-SV1), being one of the alternative KLF6 splicing isoforms, participates in tumor occurrence and development and has the potential to become a new target for molecular targeted therapy, although its action mechanism remains to be determined. The purpose of this article is to provide a comprehensive and systematic review of the important role of KLF6-SV1 in human malignant tumors to provide novel insights for oncotherapy.

摘要

Krüppel样因子6(KLF6)是特异性蛋白/Krüppel样因子(SP/KLF)转录因子家族中研究最多的成员之一。它具有典型的锌指结构,在调节细胞生物学过程中起关键作用。最近,它被认为在抗癌方面发挥作用。Krüppel样因子6剪接变体1(KLF6-SV1)作为KLF6的可变剪接异构体之一,参与肿瘤的发生和发展,尽管其作用机制尚待确定,但它有潜力成为分子靶向治疗的新靶点。本文旨在对KLF6-SV1在人类恶性肿瘤中的重要作用进行全面系统综述,为肿瘤治疗提供新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e38/8017371/34d9f3b7f044/fcell-09-661731-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e38/8017371/ce4fe8fcbfed/fcell-09-661731-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e38/8017371/669782f0f909/fcell-09-661731-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e38/8017371/d3a36abd0d06/fcell-09-661731-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e38/8017371/34d9f3b7f044/fcell-09-661731-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e38/8017371/ce4fe8fcbfed/fcell-09-661731-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e38/8017371/669782f0f909/fcell-09-661731-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e38/8017371/d3a36abd0d06/fcell-09-661731-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e38/8017371/34d9f3b7f044/fcell-09-661731-g004.jpg

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本文引用的文献

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J Cancer. 2019 Aug 29;10(22):5324-5331. doi: 10.7150/jca.34212. eCollection 2019.
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RNAi therapeutic and its innovative biotechnological evolution.RNAi 疗法及其创新生物技术的发展。
Biotechnol Adv. 2019 Sep-Oct;37(5):801-825. doi: 10.1016/j.biotechadv.2019.04.012. Epub 2019 Apr 26.
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Krüppel like factor 6 splice variant 1 (KLF6-SV1) overexpression recruits macrophages to participate in lung cancer metastasis by up-regulating TWIST1.
BMC Oral Health. 2024 Apr 30;24(1):510. doi: 10.1186/s12903-024-04250-5.
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Abnormal expression of Krüppel-like transcription factors and their potential values in lung cancer.Krüppel样转录因子的异常表达及其在肺癌中的潜在价值。
Heliyon. 2024 Mar 21;10(7):e28292. doi: 10.1016/j.heliyon.2024.e28292. eCollection 2024 Apr 15.
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miRNA‑21 promotes the progression of acute liver failure via the KLF6/autophagy/IL‑23 signaling pathway.miRNA-21 通过 KLF6/自噬/IL-23 信号通路促进急性肝衰竭的进展。
Mol Med Rep. 2024 May;29(5). doi: 10.3892/mmr.2024.13205. Epub 2024 Mar 22.
6
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Sci Adv. 2023 Nov 17;9(46):eadg8126. doi: 10.1126/sciadv.adg8126. Epub 2023 Nov 15.
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Enhanced hepatocarcinogenesis in mouse models and human hepatocellular carcinoma by coordinate KLF6 depletion and increased messenger RNA splicing.协调的 KLF6 耗竭和增加的信使 RNA 剪接增强了小鼠模型和人肝癌的肝癌发生。
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