4.6 Review

NPM2 in malignant peritoneal mesothelioma: from basic tumor biology to clinical medicine

期刊

WORLD JOURNAL OF SURGICAL ONCOLOGY
卷 20, 期 1, 页码 -

出版社

BMC
DOI: 10.1186/s12957-022-02604-3

关键词

Nucleoplasmin2; Gene structure; Malignant peritoneal mesothelioma; Molecular targeting therapy

资金

  1. General Program of the National Natural Science Foundation of China [82073376]
  2. Beijing Municipal Administration of Hospitals' Ascent Plan [DFL20180701]

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This review summarizes the gene biology features and protein structure of nucleoplasmin2 (NPM2) and explores its relationship with malignant peritoneal mesothelioma (MPM). The results show that NPM2 may play a key role in the development and progression of MPM. The expression of NPM2 is correlated with the pathology and survival rate of MPM patients.
Background This review systematically summarizes gene biology features and protein structure of nucleoplasmin2 (NPM2) and the relationship between NPM2 and malignant peritoneal mesothelioma (MPM), in order to explore the molecular pathological mechanism of MPM and explore new therapeutic targets. Methods NCBI PubMed database was used for the literature search. NCBI Gene and Protein databases, Ensembl Genome Browser, UniProt, and RCSB PDB database were used for gene and protein review. Three online tools (Consurf, DoGSiteScorer, and ZdockServer), the GEPIA database, and the Cancer Genome Atlas were used to analyze bioinformatics characteristics for NPM2 protein. Results The main structural domains of NPM2 protein include the N-terminal core region, acidic region, and motif and disordered region. The N-terminal core region, involved in histone binding, is the most conserved domain in the nucleoplasmin (NPM) family. NPM2 with a large acidic tract in its C-terminal tail (NPM2-A2) is able to bind histones and form large complexes. Bioinformatics results indicated that NPM2 expression was correlated with the pathology of multiple tumors. Among mesothelioma patients, 5-year survival of patients with low-NPM2-expression was significantly higher than that of the high-NPM2-expression patients. NPM2 can facilitate the formation of histone deacetylation. NPM2 may promote histone deacetylation and inhibit the related-gene transcription, thus leading to abnormal proliferation, invasion, and metastasis of MPM. Conclusion NPM2 may play a key role in the development and progression of MPM.

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