ArticleFrontiers in immunology2026
KRTCAP2 accelerates malignant progression through modulating tumor cell function and M2 macrophage infiltration in glioma.
Article in Frontiers in immunology, 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Aberrant glycosylation of proteins plays a critical role in promoting tumor growth and modulating immune responses within the tumor microenvironment. Keratinocyte-associated protein 2 (KRTCAP2) encodes a corresponding protein involved in N-glycosylation, yet its functional and clinical relevance in glioma remains poorly understood. This study aims to elucidate the dual functions of KRTCAP2 in glioma tumorigenesis and immune evasion, and to evaluate its potential as a prognostic biomarker. Methods: We employed bioinformatics analysis to evaluate KRTCAP2 mRNA expression patterns and immune microenvironment scores in glioma. Multiplex immunohistochemistry (mlHC) was utilized to assess KRTCAP2 protein expression, its association with clinical features, patient prognosis, and immune cell infiltration. To assess the function of KRTCAP2 in regulating glioma cell behaviors and its influence on the tumor immune microenvironment, a set of Results: KRTCAP2 mRNA and protein levels were markedly upregulated in glioma tissues compared to non-tumorous brain tissues. Elevated KRTCAP2 protein expression correlated with adverse clinical characteristics and reduced overall survival. Notably, KRTCAP2 expression showed a significant positive association with the density of infiltrating CD68+ and CD163+ tumor-associated macrophages (TAMs). Depletion of KRTCAP2 significantly inhibited the proliferative, migratory, and invasive capacities of glioma cells, confirming its role as an oncogenic driver. Conversely, KRTCAP2 overexpression promoted these malignant behaviors. Drug sensitivity analysis suggested a role for KRTCAP2 in chemoresistance, with targeted inhibition enhancing glioma cell responsiveness to temozolomide (TMZ). Conclusions: Our findings identify KRTCAP2 as a novel prognostic biomarker in glioma, with potential utility in predicting immunotherapy response. The study highlights its clinical significance and multifaceted role in shaping an immunosuppressive glioma microenvironment, underscoring KRTCAP2 as a promising therapeutic target.
Indexed as
Identifiers
What 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.