ArticleJournal of experimental & clinical cancer research : CR2026
Epitranscriptomic silencing of the ZC3H13/m
Article in Journal of experimental & clinical cancer research : CR, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Beyond mBiomedicines · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
backgroundThe immunosuppressive tumor microenvironment (TME) is a cardinal driver of immune escape and resistance to immunotherapy in renal cell carcinoma (RCC). The N6-methyladenosine (m
methodsLoss- and gain-of-function studies were performed in vitro and in allograft tumor model. Tumor-infiltrating immune cells were profiled with flow cytometry and immunostaining. The pivotal cytokine mediated by ZC3H13 depletion was identified through an integrated analysis of RNA-seq and PCR array. The molecular target of ZC3H13 was elucidated through integrated m
resultsLow ZC3H13 expression was an independent predictor of poor prognosis in RCC. Functionally, ZC3H13 silencing enhanced the malignant behaviors of RCC cells and drove an immunosuppressive microenvironment characterized by aberrant recruitment of myeloid-derived suppressor cells (MDSCs). Mechanistically, ZC3H13 promoted m
conclusionWe identified that ZC3H13 loss unleashes the NF-κB-CSF2 signaling cascade via m
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.