ArticleTranslational oncology2025
miR-4537 curtails ferroptosis by targeting MIOX in renal cell carcinoma.
Article in Translational oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Reading the tumour at single-cell resolution: Original research in the Precision Therapeutics special issue.Translational oncology · 2026Article
- miR-135a-5p exerts tumor-suppressive effects in 769P renal carcinoma cells through the TFAP2A/KRT8 signaling axis.In vitro cellular & developmental biology. Animal · 2026Article
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
No grant is acknowledged in the PubMed record.
Abstract
Ferroptosis, an iron-dependent mode of cell death, has gained prominence for its critical role in the advancement of various cancers, notably clear cell renal carcinoma (ccRCC). The intricacies of ferroptosis's involvement in ccRCC, however, remain largely undefined. This study aimed to dissect the contribution of ferroptosis to ccRCC by examining differentially expressed genes (DEGs) identified within the TCGA ccRCC database and ferroptosis driver genes catalogued in the FerrDb database (dedicates to ferroptosis regulators and ferroptosis-disease associations). We employed 786-O and ACHN ccRCC cell lines, alongside HK2 (human kidey-2) cells and HKC (human kidney cells), to confirm the expression of 9 shared genes. Among these, MIOX (myo-inositol oxygenase) emerged as significantly downregulated in ccRCC cells compared to HK2 and HKC cells. Subsequent survival analysis illuminated a positive correlation between MIOX expression and improved patient survival, underscoring its prognostic significance. Further investigations into MIOX regulation identified four miRNAs via TargetScan predictions, with miR-4537 significantly upregulated in ccRCC cell lines. Functional assays involving miR-4537 mimics and inhibitors, combined with ferroptosis inducers and inhibitors, elucidated its impact on ccRCC cell growth and ferroptosis modulation. The results revealed that miR-4537 expression was diminished following ferroptosis induction, and the miR-4537 inhibitor markedly curbing ccRCC cell proliferation by fostering ferroptosis, while the mimic exerted opposite effects. Mechanistically, miR-4537 targets the 3'-UTR of MIOX to manipulate its expression, ultimately inhibiting ferroptosis in ccRCC cells. Our research indicated that miR-4537 restrained ferroptosis by regulating MIOX in ccRCC, offering novel insights into the mechanisms of ferroptosis in cancer biology and highlighting latent therapeutic avenues for cancer treatment through ferroptosis modulation.
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.