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靶向 NAP1L5 联合 MYH9 通过 PI3K/AKT/mTOR 信号通路抑制 HCC 进展。

NAP1L5 targeting combined with MYH9 Inhibit HCC progression through PI3K/AKT/mTOR signaling pathway.

机构信息

Guizhou Medical University, Guiyang, Guizhou 550001, China.

Department of Hepatobiliary Surgery, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550001, China.

出版信息

Aging (Albany NY). 2022 Nov 11;14(22):9000-9019. doi: 10.18632/aging.204377.

DOI:10.18632/aging.204377
PMID:36374212
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9740361/
Abstract

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer death worldwide. Nucleosome assembly protein 1-like 5 (NAP1L5) is a protein-coding gene that encodes a protein similar to nucleosome assembly protein 1 (NAP1). It is a histone chaperone that plays an important role in gene transcription in organisms. However, the role of NAP1L5 in the pathogenesis of hepatocellular carcinoma remains to be elucidated. In this study, low expression of NAP1L5 was found in hepatocellular carcinoma, and the downregulation of NAP1L5 was related to shorter survival and disease-free survival. In addition, its expression is also related to the tumor size and recurrence of hepatocellular carcinoma. The overexpression and knockdown of NAP1L5 by plasmid and siRNA showed that NAP1L5 inhibited the proliferation, migration and invasion and induced apoptosis of hepatoma cells. experiments confirmed that NAP1L5 can inhibit the growth and metastasis of hepatocellular carcinoma cells. In the mechanistic study, we found that NAP1L5 affects the occurrence and development of hepatocellular carcinoma by regulating MYH9 to inhibit the PI3K/AKT/mTOR signaling pathway. As a functional tumor suppressor, NAP1L5 is expressed at low levels in HCC. NAP1L5 inhibits the PI3K/AKT/mTOR signaling pathway in hepatocellular carcinoma by regulating MYH9. It may be a new potential target for liver cancer treatment.

摘要

肝细胞癌 (HCC) 是全球癌症死亡的主要原因之一。核小体组装蛋白 1 样 5 (NAP1L5) 是一种编码蛋白的基因，该蛋白类似于核小体组装蛋白 1 (NAP1)。它是一种组蛋白伴侣，在生物体内的基因转录中发挥重要作用。然而，NAP1L5 在肝细胞癌发病机制中的作用仍有待阐明。在这项研究中，发现肝细胞癌中 NAP1L5 的表达降低，NAP1L5 的下调与较短的生存和无病生存有关。此外，其表达也与肝癌的肿瘤大小和复发有关。通过质粒和 siRNA 过表达和敲低 NAP1L5 表明，NAP1L5 抑制肝癌细胞的增殖、迁移和侵袭，并诱导细胞凋亡。实验证实 NAP1L5 可抑制肝癌细胞的生长和转移。在机制研究中，我们发现 NAP1L5 通过调节 MYH9 抑制 PI3K/AKT/mTOR 信号通路，影响肝细胞癌的发生和发展。作为一种功能性肿瘤抑制因子，NAP1L5 在 HCC 中的表达水平较低。NAP1L5 通过调节 MYH9 抑制 PI3K/AKT/mTOR 信号通路在肝细胞癌中发挥作用。它可能是肝癌治疗的一个新的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b6e/9740361/974cbc382257/aging-14-204377-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b6e/9740361/88dfe263dcba/aging-14-204377-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b6e/9740361/a9a3a3b8d67b/aging-14-204377-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b6e/9740361/cdc36d007ab2/aging-14-204377-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b6e/9740361/bc4166e3dd2c/aging-14-204377-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b6e/9740361/c4aa457a2081/aging-14-204377-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b6e/9740361/75910cbb2cdf/aging-14-204377-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b6e/9740361/8120bd730217/aging-14-204377-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b6e/9740361/bb530281ee1b/aging-14-204377-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b6e/9740361/974cbc382257/aging-14-204377-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b6e/9740361/88dfe263dcba/aging-14-204377-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b6e/9740361/a9a3a3b8d67b/aging-14-204377-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b6e/9740361/cdc36d007ab2/aging-14-204377-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b6e/9740361/bc4166e3dd2c/aging-14-204377-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b6e/9740361/c4aa457a2081/aging-14-204377-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b6e/9740361/75910cbb2cdf/aging-14-204377-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b6e/9740361/8120bd730217/aging-14-204377-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b6e/9740361/bb530281ee1b/aging-14-204377-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b6e/9740361/974cbc382257/aging-14-204377-g009.jpg

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NAP1L5 targeting combined with MYH9 Inhibit HCC progression through PI3K/AKT/mTOR signaling pathway.

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引用本文的文献

[1]
NAP1L5 in acute myeloid leukemia: a prognostic biomarker and potential therapeutic target.

Front Oncol. 2025-7-25

[2]
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J Alzheimers Dis Rep. 2025-1-13

[3]
Non-Muscle Myosin II A: Friend or Foe in Cancer?

Int J Mol Sci. 2024-8-30

[4]
Altered methylation of imprinted genes in neuroblastoma: implications for prognostic refinement.

J Transl Med. 2024-8-31

[5]
Unveiling the enigmatic role of MYH9 in tumor biology: a comprehensive review.

Cell Commun Signal. 2024-8-27

[6]
Exploring the nexus between MYH9 and tumors: novel insights and new therapeutic opportunities.

Front Cell Dev Biol. 2024-8-1

[7]
Epigenetic silencing promotes pancreatic cancer growth by activating Wnt signaling.

Cancer Biol Ther. 2024-12-31

[8]
MALAT1-regulated gene expression profiling in lung cancer cell lines.

BMC Cancer. 2023-9-4

本文引用的文献

[1]
Targeting the PI3K/Akt/mTOR Pathway in Hepatocellular Carcinoma.

Biomedicines. 2021-11-8

[2]
Role of Forkhead Box O Proteins in Hepatocellular Carcinoma Biology and Progression (Review).

Front Oncol. 2021-5-27

[3]
Global Cancer Statistics 2020: GLOBOCAN Estimates of Incidence and Mortality Worldwide for 36 Cancers in 185 Countries.

CA Cancer J Clin. 2021-5

[4]
Targeting CREB in Cancer Therapy: A Key Candidate or One of Many? An Update.

Cancers (Basel). 2020-10-28

[5]
Silencing MYH9 blocks HBx-induced GSK3β ubiquitination and degradation to inhibit tumor stemness in hepatocellular carcinoma.

Signal Transduct Target Ther. 2020-2-14

[6]
Low MYH9 expression predicts a good prognosis for hepatocellular carcinoma.

Int J Clin Exp Pathol. 2018-5-1

[7]
Nucleosome assembly proteins NAP1L1 and NAP1L4 modulate p53 acetylation to regulate cell fate.

Biochim Biophys Acta Mol Cell Res. 2019-10-18

[8]
LncRNA CDKN2B-AS1 promotes tumor growth and metastasis of human hepatocellular carcinoma by targeting let-7c-5p/NAP1L1 axis.

Cancer Lett. 2018-8-27

[9]
MYH9: Structure, functions and role of non-muscle myosin IIA in human disease.

Gene. 2018-4-19

[10]
PRDM8 exhibits antitumor activities toward hepatocellular carcinoma by targeting NAP1L1.

Hepatology. 2018-5-21

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