ArticleOncology reports2025
HOTTIP suppresses ferroptosis via mediating DGCR8/miR‑214‑3p/GPX4 regulatory axis in osteosarcoma.
Article in Oncology reports, 2025. 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
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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.
- The HOXA gene cluster: a critical regulator in bone-related disorders.Annals of medicine · 2026Review
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteosarcoma (OS) is the most common primary bone malignancy in children and adolescents and the current typical strategy remains unsatisfactory in clinical practice. Ferroptosis has been considered as a novel form of programmed cell death in eukaryotic cells, which is characterized by iron‑dependent lipid peroxidation accumulation. The emergence of ferroptosis brings great hope to develop the potential therapeutic targets for OS patients. Long noncoding (lnc)RNA HOXA transcript at the distal tip (HOTTIP) has been identified as an oncogene to facilitate tumorigenesis in OS. Whether ferroptosis participates in this lncRNA mediated OS tumorigenesis is not fully understood. In the present study, HOTTIP was found to be downregulated in the Erastin‑treated OS cells. Silence of HOTTIP promoted, while ectopic expression of HOTTIP suppressed, ferroptosis in OS cells
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