Journal
SCIENTIFIC REPORTS
Volume 12, Issue 1, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41598-022-12862-6
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Funding
- Basic Research Project of Shenzhen Knowledge Innovation Plan [JCY20170307112807219]
- Shenzhen HighLevel Hospital Construction Plan
- Hospital Research Project [SZ2020QN002, SZ2020QN020]
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This study found that NCAPH is overexpressed in lung adenocarcinoma (LUAD) and is associated with prognosis and immune infiltrates. High expression of NCAPH is associated with shorter overall survival and decreased progression-free interval and disease-specific survival. In addition, NCAPH is associated with several gene sets and immune cell levels. Knocking down NCAPH can inhibit the malignant phenotype of LUAD cells in vitro.
Non-SMC condensin I complex subunit H (NCAPH) plays a regulatory role in various cancers. However, its role in prognosis and immune infiltrates in lung adenocarcinoma (LUAD) remains unclear. This study examined the expression of NCAPH in tumor tissues and its association with immune infiltrates and prognostic roles in LUAD patients. Patients characteristics were obtained from The Cancer Genome Atlas (TCGA). Integrated analysis of TCGA showed that NCAPH was overexpressed across cancers, including LUAD. NCAPH expression was verified by quantitative polymerase chain reaction and western blotting in 20 LUAD matched tissues. High NCAPH expression was significantly related to T, N, M, pathologic stage, primary therapy outcome and smoking status according to the Wilcoxon rank sum test. Cox and Kaplan-Meier analyses showed that the NCAPH-high group was associated with shorter OS. The PFI and DSS in the NCAPH-high group were significantly decreased. Multivariate analysis showed that NCAPH was an independent predictive factor for poor prognosis. Gene set enrichment analysis demonstrated that the G2/M checkpoint, ncRNA metabolic, memory B cells, KRAS, E2F targets and MIER1 process were significantly associated with NCAPH expression. Single-sample Gene Set Enrichment Analysis indicated that NCAPH expression was associated with levels of Th2 and mast cells. The impact of NCAPH on malignant phenotypes was evaluated by MTT, transwell, cell cycle and apoptosis assays in vitro. The malignant phenotype of LUAD cells was inhibited if NCAPH was knocked down. In conclusion, this research indicates that NCAPH could be a potential factor for predicting prognosis and a new biomarker in LUAD.
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