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NME2通过4EBP1磷酸化和自噬调节来调控肝癌进展，且不依赖于mTOR。

NME2 modulates HCC progression through 4EBP1 phosphorylation and autophagy regulation independent of mTOR.

作者信息

Chen Wei, Zhou Da-Chen, Rui Chen-Hui, Wang Rong, Shan Sheng-Liang, Chen Jiang-Ming, Luo Wen-Wu, Cui Xiao, Hou Hui, Liu Fu-Bao

机构信息

Department of General Surgery, The Second People's Hospital of Hefei, Anhui, China.

Department of Liver Transplantation, The Second Affiliated Hospital of Anhui Medical University, Anhui, China.

出版信息

Hepatol Commun. 2025 Jun 9;9(7). doi: 10.1097/HC9.0000000000000715. eCollection 2025 Jul 1.

DOI:10.1097/HC9.0000000000000715
PMID:40489759
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12150935/
Abstract

BACKGROUND

To investigate the role of nucleoside diphosphate kinase 2 (NME2) in HCC progression, assessing its therapeutic potential.

METHODS

Utilizing transcriptome sequencing data from The Cancer Genome Atlas (TCGA) and immunohistochemical staining of tissue microarrays, we analyzed NME2 expression in HCC tumor tissues. The effects of NME2 on HCC cell proliferation and autophagy flux were assessed through knockdown and overexpression experiments. Additionally, the relationship between NME2 and 4EBP1 phosphorylation was explored through specific site mutation analysis.

RESULTS

NME2 overexpression in HCC correlated with poor prognosis. NME2 knockdown significantly hindered HCC cell proliferation and induced autophagy flux. Notably, NME2 modulates 4EBP1 phosphorylation (Thr37/46) independently of mTOR, unveiling a novel axis in HCC pathogenesis. Additionally, NME2 modulates eukaryotic translation initiation factor 4F (eIF4F) complex formation and autophagy flux.

CONCLUSIONS

NME2 plays a crucial role in HCC development by modulating 4EBP1 phosphorylation and autophagy through an mTOR-independent pathway. Our research underscores NME2's significance as a potential therapeutic target in HCC, meriting further exploration of its underlying mechanisms and clinical applicability.

摘要

背景

研究核苷二磷酸激酶2（NME2）在肝癌进展中的作用，评估其治疗潜力。

方法

利用来自癌症基因组图谱（TCGA）的转录组测序数据和组织微阵列的免疫组织化学染色，我们分析了肝癌肿瘤组织中NME2的表达。通过敲低和过表达实验评估NME2对肝癌细胞增殖和自噬通量的影响。此外，通过特定位点突变分析探索NME2与4EBP1磷酸化之间的关系。

结果

肝癌中NME2过表达与预后不良相关。NME2敲低显著阻碍肝癌细胞增殖并诱导自噬通量。值得注意的是，NME2独立于mTOR调节4EBP1磷酸化（Thr37/46），揭示了肝癌发病机制中的一个新轴。此外，NME2调节真核翻译起始因子4F（eIF4F）复合物的形成和自噬通量。

结论

NME2通过不依赖mTOR的途径调节4EBP1磷酸化和自噬，在肝癌发展中起关键作用。我们的研究强调了NME2作为肝癌潜在治疗靶点的重要性，值得进一步探索其潜在机制和临床适用性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2ab/12150935/231110bcd92f/hc9-9-e0715-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2ab/12150935/5c5b57dc53bf/hc9-9-e0715-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2ab/12150935/d31c5e254506/hc9-9-e0715-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2ab/12150935/792d1cf649d9/hc9-9-e0715-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2ab/12150935/4d99a9858fce/hc9-9-e0715-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2ab/12150935/231110bcd92f/hc9-9-e0715-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2ab/12150935/5c5b57dc53bf/hc9-9-e0715-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2ab/12150935/d31c5e254506/hc9-9-e0715-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2ab/12150935/792d1cf649d9/hc9-9-e0715-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2ab/12150935/4d99a9858fce/hc9-9-e0715-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2ab/12150935/231110bcd92f/hc9-9-e0715-g005.jpg

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