ArticleJournal of inflammation research2025
CKS2 Mediates Hepatocellular Carcinoma Recurrence After Hepatic Ischemia-Reperfusion Injury Related to M2 Macrophages.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Hepatocellular carcinoma (HCC) recurrence remains a significant burden on global healthcare. Hepatic ischemia-reperfusion injury (HIRI) is a common complication in liver surgery and may be a contributing factor to HCC recurrence. Nevertheless, the potential mechanism underlying HIRI-induced HCC recurrence has not been fully elucidated. Herein, by combining bioinformatics approaches and basic experimental research, CKS2 was preliminarily identified as a crucial factor involved in HIRI-induced HCC recurrence potentially by modulating M2 macrophages. Methods: Through performing Weighted Gene Co-Expression Network Analysis (WGCNA), differential gene expression analysis, and screening for genes associated with disease-free survival (DFS) on large-scale genomics projects including The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), the pivotal role of CKS2 in HIRI-induced HCC recurrence was determined. The clinical significance, single-cell analysis, immune cell infiltration correlation, functional enrichment, mutation landscape, and drug sensitivity of CKS2 in HCC were further characterized. Finally, CKS2 expression and function were validated through experimental techniques such as flow cytometry, immunohistochemistry, Western blot assay and quantitative real-time PCR (qRT-PCR). Results: The expression of CKS2 was significantly upregulated in HIRI and HCC tissues and was closely associated with adverse clinical outcomes in HCC patients. There was a positive correlation between CKS2 expression and tumor stemness characteristics. Additionally, high CKS2 expression was strongly linked to M2 macrophage infiltration in HCC tissues. And drug sensitivity analysis indicated that HCC patients with high CKS2 expression were prone to develop drug resistance, complicating clinical anti-tumor treatment. Ultimately, the expression pattern of CKS2 and its correlation with M2 macrophages in HCC were confirmed through experimental validation. Conclusion: CKS2 was identified as a key factor in HIRI-induced HCC recurrence and was critically associated with M2 macrophage infiltration abundance, providing novel insights and a direction for future research.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.