更新于：2024-09-19

KLF7

更新于：2024-09-19

基本信息

别名

KLF7、Krueppel-like factor 7、Kruppel like factor 7

+ [2]

简介

Transcriptional factor (PubMed:9774444, PubMed:16339272). Plays a critical role in neuronal morphogenesis and survival of sensory neurons (By similarity). Represses the corneal epithelium differentiation (PubMed:28916725). Acts also as a metabolic regulator, by modulating insulin sensitivity in pancreatic beta cells and skeletal muscle cells (PubMed:16339272). Inhibits transcriptional inducers of adipogenesis and has a repressive role in the expression of several adipokines, including leptin (PubMed:16339272).

关联

100 项与 KLF7 相关的临床结果

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100 项与 KLF7 相关的转化医学

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0 项与 KLF7 相关的专利（医药）

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190

项与 KLF7 相关的文献（医药）

2024-12-31·Cancer Biology & Therapy

KLF7 enhances the invasion and migration of colorectal cancer cells via the miR-139-5p/TPD52 axis

Article

作者: Han, Jiaxu ; Niu, Wenbo ; Zhang, Juan ; Li, Zhihan ; Meng, Qingyu ; Tian, Zhongtao

In this study, we aimed to investigate the molecular mechanism of Krüppel-like factor 7 (KLF7) in colorectal cancer (CRC) cell invasion and migration. The expression pattern of KLF7 in CRC tissues and the correlation between KLF7 expression and clinical symptoms of CRC were analyzed. CRC cell lines were transfected with si-KLF7, followed by qRT-PCR or western blot detection of KLF7, miR-139-5p, and tumor protein D52 (TPD52) expression, cell counting kit-8 (CCK-8) assay to detect cell viability, and transwell detection of invasion and migration. Chromatin immunoprecipitation (ChIP) analyzed the enrichment KLF7 in the miR-139-5p promoter. The dual-luciferase reporter assay verified the binding relationship between KLF7 and miR-139-5p, and between miR-139-5p and TPD52. In the subcutaneous tumorigenesis experiment, tumor growth was observed and ki67-positive expression was detected. KLF7 is abundantly expressed in CRC cells KLF7 silencing inhibits CRC cell viability, invasion, and migration. KLF7 represses miR-139-5p expression by binding to the miR-139-5p promoter. miR-139-5p targets TPD52 expression. miR-13-5p inhibition or TPD52 overexpression partially counteracted the effect of KLF7 silencing in CRC cells. KLF7 silencing suppresses tumor growth in vivo. In conclusion, KLF7 suppresses miR-139-5p expression by binding to the miR-139-5p promoter, thereby upregulating TPD52 expression and enhancing CRC cell invasion and migration.

2024-09-01·General and Comparative Endocrinology

Comparative analysis of Krüppel-like factors expression in the retinas of zebrafish and mice during development and after injury

Article

作者: Urban-Sosa, Valeria A ; Lazcano, Iván ; Luna, Maricela ; Ávila-Mendoza, José ; Orozco, Aurea ; Martínez-Moreno, Carlos G ; Arámburo, Carlos

The Krüppel-like factors (KLFs) have emerged as important transcriptional regulators of various cellular processes, including neural development. Some of them have been described as intrinsic factors involved in axon regeneration in the central nervous system (CNS) of vertebrates. Zebrafish are known for their ability to regenerate several tissues in adulthood, including the CNS, a capability lost during vertebrate evolution and absent in adult mammals. The role that KLFs could play in this differential ability remains unknown. Therefore, in this study, we analyzed the endogenous response of certain KLFs implicated in axon regeneration (KLFs 6, 7, 9, and 13) during retina development and after axon injury. The results showed that the expression of Klfs 6, 7, and 13 decreases in the developing retina of mice but not in zebrafish, while the mRNA levels of Klf9 strongly increase in both species. The response to injury was further analyzed using optic nerve crush (ONC) as a model of lesion. Our analysis during the acute phase (hours) demonstrated an induction of Klfs 6 and 7 expression exclusively in the zebrafish retina, while Klfs 9 and 13 mRNA levels increased in both species. Further analysis of the chronic response (days) showed that mRNA levels of Klf6 transiently increase in the retinas of both zebrafish and mice, whereas those of Klf7 decrease later after optic nerve injury. In addition, the analysis revealed that the expression of Klf9 decreases, while that of Klf13 increases in the retinas of zebrafish in response to optic nerve injury but remains unaltered in mice. Altogether, these findings support the hypothesis that KLFs may play a role in the differential axon regeneration abilities exhibited by fish and mice.

2024-09-01·The FEBS Journal

KLF7 promotes neuroblastoma differentiation through the GTPase signaling pathway by upregulating neuroblast differentiation‐associated protein AHNAKs and glycerophosphodiesterase GDPD5

Article

作者: Shi, Lei ; Xia, Yang ; Song, Yue ; Xie, Li ; Zhang, Xue ; Song, Huilin ; Zhang, Jiahui ; Jing, Wenwen ; Jia, Ying ; Meng, Lingdi ; Cao, Tianhua ; Qiao, Shupei

The arrest of neural crest‐derived sympathoadrenal neuroblast differentiation contributes to neuroblastoma formation, and overriding this blocked differentiation is a clear strategy for treating high‐risk neuroblastoma. A better understanding of neuroblast or neuroblastoma differentiation is essential for developing new therapeutic approaches. It has been proposed that Krueppel‐like factor 7 (KLF7) is a neuroblastoma super‐enhancer‐associated transcription factor gene. Moreover, KLF7 was found to be intensely active in postmitotic neuroblasts of the developing nervous system during embryogenesis. However, the role of KLF7 in the differentiation of neuroblast or neuroblastoma is unknown. Here, we find a strong association between high KLF7 expression and favorable clinical outcomes in neuroblastoma. KLF7 induces differentiation of neuroblastoma cells independently of the retinoic acid (RA) pathway and acts cooperatively with RA to induce neuroblastoma differentiation. KLF7 alters the GTPase activity and multiple differentiation‐related genes by binding directly to the promoters of neuroblast differentiation‐associated protein (AHNAK and AHNAK2) and glycerophosphodiester phosphodiesterase domain‐containing protein 5 (GDPD5) and regulating their expression. Furthermore, we also observe that silencing KLF7 in neuroblastoma cells promotes the adrenergic‐to‐mesenchymal transition accompanied by changes in enhancer‐mediated gene expression. Our results reveal that KLF7 is an inducer of neuroblast or neuroblastoma differentiation with prognostic significance and potential therapeutic value.

项与 KLF7 相关的新闻（医药）

2024-03-10

·今日头条

新策略！中山大学研究人员发文：促进癌症进展和转移的机制

本文为转化医学网原创，转载请注明出处作者：Sophia 导读：头颈部鳞状癌（HNSCC）以其高侵袭性和对颈部淋巴结转移的易感性而闻名，这极大地导致了其预后不良。在肿瘤发生过程中，许多类型的癌细胞获得致癌超增强子（SE），从而驱动癌基因的过表达，从而维持恶性进展。 2024年3月5日，中山大学侯劲松、王成共同通讯在《Journal of Experimental & Clinical Cancer Research》上发表题为“KLF7 regulates super-enhancer-driven IGF2BP2 overexpression to promote the progression of head and neck squamous cell carcinoma”的研究论文，我们鉴定了胰岛素样生长因子 2 mRNA 结合蛋白 2 （IGF2BP2）作为 HNSCC 中的枢纽 SE 相关基因。我们观察到IGF2BP2表达的显著上调，这促进了 HNSCC 的致瘤性和转移。 https://jeccr-biomedcentral-com.libproxy1.nus.edu.sg/articles/10.1186/s13046-024-02996-y 研究背景 01 头颈癌包括各种组织学类型，其中鳞状细胞癌是最常见的。头颈部鳞状细胞癌（HNSCC）具有高度侵袭性，容易发生转移性颈部淋巴结（CLN），导致复发和转移的风险较高，是死亡的主要原因。尽管诊断和治疗方法取得了进步，但在过去 30 年中，HNSCC 患者的 5 年生存率没有显着提高，仍保持在 50% 左右。因此，了解HNSCC侵袭性转移的调控机制对于开发创新的治疗策略和改善患者的预后至关重要。由遗传和表观遗传改变驱动的癌基因的异常转录在癌症的致瘤性和转移性中起着关键作用。最近的证据表明，超级增强子（SEs）是重要的非编码调控元件，可决定不同细胞类型的身份。SE增强基因的表达，这些基因在生物体发育和疾病进展过程中对维持细胞身份至关重要。SE 是 DNA 顺式调节元件，具有卓越的转录活性，是由多个相邻增强子组成的簇。SE 主要由转录激活相关的组蛋白修饰（组蛋白 3 赖氨酸 27 乙酰化，H3K27Ac;组蛋白 3 赖氨酸 4 单甲基化，H3K4me1）、辅因子（含溴结构域的蛋白 4、BRD4、介质复合物亚基 1、MED1）、染色质调节因子（p300）、RNA 聚合酶 II （RNA Pol II）和细胞类型特异性转录因子（TF）通过染色质免疫沉淀测序（ChIP-seq）进行定义。一些研究利用超级增强子排名（ROSE）算法来识别不同类型癌症中的 SE。这些研究证实，SE负责调节癌症发展过程中重要癌基因（如CCAT1、TP63、MYC、SOX2、KLF5和FOSL1）的过表达。这种调节有助于维持癌细胞的特征并促进其恶性进展。 SE是在控制基因表达和细胞功能方面起着至关重要作用的基因组区域。有研究表明，在不同的细胞环境中，SE相关转录的抑制优先调节重要的癌细胞或组织特异性基因。目前，通过破坏SE或抑制SE相关转录程序直接靶向SE的治疗策略已在各种癌症中显示出有希望的结果。研究结果 02 在此，我们的研究将IGF2BP2确定为枢纽SE相关基因，在HNSCC组织中表现出异常表达。观察到 IGF2BP2 表达增加与 HNSCC 患者的恶性进展和不良预后有关。体外和体内实验均证实，IGF2BP2通过促进细胞增殖、迁移和侵袭来促进HNSCC的致瘤性和转移。从机制上讲， IGF2BP2-SE 区域显示出 H3K27Ac、BRD4 和 MED1 的富集，这导致通过失活 SE 相关转录程序来抑制IGF2BP2转录和表达。此外，还发现KLF7诱导IGF2BP2转录并直接与其启动子和SE区域结合。KLF7丰度与HNSCC中IGF2BP2丰度呈正相关。KLF7 和 IGF2BP2 高表达的患者预后较差。最后，我们证明了靶向BRD4的小分子抑制剂JQ1减弱了HNSCC细胞的增殖和转移能力。 KLF7调控SE驱动的IGF2BP2过表达促进HNSCC恶性进展的机制模型。总之，我们的研究揭示了 SE 和 KLF7 介导的IGF2BP2过表达在促进 HNSCC 进展中的关键作用。靶向 SE 相关转录程序可能代表了管理 HNSCC 的潜在治疗策略。研究结论 03 综上所述，我们的研究揭示了IGF2BP2作为SE相关基因在促进HNSCC恶性进展中的临床和生物学功能。在机制方面，我们观察到 SE 驱动的 IGF2BP2 表达通过 KLF7 以及其他转录元件（如 BRD4 和 MED1）的参与而发生转录激活。这些元素在IGF2BP2转录的异常成瘾中起作用。此外，我们还提供了证据来支持这样一种观点，即靶向 SE 驱动的转录程序可以作为治疗干预的有效策略。这些发现有可能为探索旨在根除HNSCC的创新预后生物标志物和治疗方法提供有价值的临床证据。参考资料： https://jeccr-biomedcentral-com.libproxy1.nus.edu.sg/articles/10.1186/s13046-024-02996-y 注：本文旨在介绍医学研究进展，不能作为治疗方案参考。如需获得健康指导，请至正规医院就诊。热门·直播/活动 🕓 上海｜06月14日-16日 ▶ 第六届上海国际癌症大会将于6月14-16日在上海举办，学科交叉，共同推进肿瘤研究与诊治多模态！ 🕓 北京｜09月20日-21日 ▶ 第五届单细胞技术应用研讨会暨空间组学前沿研讨会欢迎您的参与！点击对应文字查看详情

信使RNA临床1期临床终止