ArticleInternational urology and nephrology2026
Single-cell analysis reveals the molecular regulatory mechanisms of high mobility group box 1 in prostate cancer development and progression.
Article in International urology and nephrology, 2026. 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
6 authors.
Funding
Abstract
High mobility group box 1 (HMGB1), which plays a crucial role in cancer progression, remains incompletely elucidated due to the high heterogeneity and complex tumor microenvironment of prostate cancer (PCa). This study, through single-cell transcriptomic analysis, provided a comprehensive elucidation of cellular heterogeneity in PCa tissues and revealed the essential role of HMGB1 in the progression of PCa by using in vitro cell experiments. Single-cell analysis revealed that an epithelial subpopulation with high levels of HMGB1 (HMGB1+ Malignant LE) significantly increased in PCa tissues, which was closely correlated with the malignant characteristics of the tumor. KEGG enrichment analysis revealed that pathways associated with autophagy, mitophagy, and apoptosis were significantly enriched in the HMGB1+ Malignant LE sub-group. In vitro cell experiments further confirmed that knocking down HMGB1 significantly inhibited the proliferation, migration, and invasive capacity of PCa cells, while inducing cellular apoptosis and cell cycle arrest. These findings suggest that HMGB1 promotes PCa malignancy by modulating tumor cell metabolism and cellular cycle progression. This study provides novel insights into the role of HMGB1 in PCa and lays theoretical groundwork for the development of therapeutic strategies targeting HMGB1.
Indexed as
Identifiers
42430095What Socratic 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 Socratic graph.