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组蛋白去乙酰化酶 8 促进结直肠癌肝转移 通过抑制干扰素调节因子 1 和上调孤啡肽受体 1。

HDAC8 Promotes Liver Metastasis of Colorectal Cancer Inhibition of IRF1 and Upregulation of SUCNR1.

机构信息

Laboratory Medicine, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, China.

Research Center of Medical Sciences, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, China.

出版信息

Oxid Med Cell Longev. 2022 Aug 16;2022:2815187. doi: 10.1155/2022/2815187. eCollection 2022.

DOI:10.1155/2022/2815187
PMID:36035205
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9400431/
Abstract

Histone deacetylases (HDACs) are well-characterized for their involvement in tumor progression. Herein, the current study set out to unravel the association of HDAC8 with colorectal cancer (CRC). Bioinformatics analyses were carried out to retrieve the expression patterns of HDAC8 in CRC and the underlying mechanism. Following expression determination, the specific roles of HDAC8, IRF1, and SUCNR1 in CRC cell functions were analyzed following different interventions. Additionally, tumor formation and liver metastasis in nude mice were operated to verify the fore experiment. Bioinformatics analyses predicted the involvement of the HDAC8/IRF1/SUCNR1 axis in CRC. cell experiments showed that HDAC8 induced the CRC cell growth by reducing IRF1 expression. Meanwhile, IRF1 limited SUCNR1 expression by binding to its promoter. SUCNR1 triggered the growth and metastasis of CRC by inhibiting cell autophagy. HDAC8 blocked IRF1-mediated SUCNR1 inhibition and thereby inhibited autophagy, accelerating CRC cell growth. Lastly, HDAC8 facilitated the development of CRC and liver metastasis by regulating the IRF1/SUCNR1 axis . Taken together, our findings highlighted the critical role for the HDAC8/IRF1/SUCNR1 axis in the regulation of autophagy and the resultant liver metastasis in CRC.

摘要

组蛋白去乙酰化酶（HDACs）在肿瘤进展中的作用已得到充分研究。本研究旨在探讨 HDAC8 与结直肠癌（CRC）的关系。通过生物信息学分析，检索了 HDAC8 在 CRC 中的表达模式及其潜在机制。在确定表达水平后，通过不同干预措施分析了 HDAC8、IRF1 和 SUCNR1 在 CRC 细胞功能中的特定作用。此外，还在裸鼠中进行了肿瘤形成和肝转移实验，以验证前期实验。生物信息学分析预测了 HDAC8/IRF1/SUCNR1 轴在 CRC 中的参与。细胞实验表明，HDAC8 通过降低 IRF1 的表达来诱导 CRC 细胞生长。同时，IRF1 通过结合其启动子限制 SUCNR1 的表达。SUCNR1 通过抑制细胞自噬来触发 CRC 细胞的生长和转移。HDAC8 通过阻断 IRF1 介导的 SUCNR1 抑制来抑制自噬，从而加速 CRC 细胞的生长。最后，HDAC8 通过调节 IRF1/SUCNR1 轴促进 CRC 的发展和肝转移。综上所述，我们的研究结果强调了 HDAC8/IRF1/SUCNR1 轴在自噬调节和 CRC 肝转移中的关键作用。

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