ArticleJournal of translational medicine2025
Hsa_circ_0002301 inhibits ferroptosis in gastric cancer by encoding the de novo protein HECTD1-463aa.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- The m6A-circRNA axis: a therapeutic prospect for gastric cancer.Cell biology and toxicology · 2026Review
- Recent advances of circular RNAs in gastrointestinal cancer.World journal of clinical oncology · 2025Review
- Review
- Upregulated Circular RNAs in Gastric Cancer: Target Identification and Tools for Therapeutic Intervention.Cancer genomics & proteomicsReview
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
backgroundCircRNAs are closely related to ferroptosis in gastric cancer cells; however, the mechanism by which circRNAs regulate ferroptosis in gastric carcinogenesis remains unknown. CircRNA-encoded novel peptides are functional products translated from the open reading frames (ORFs) within circular RNAs, demonstrating that circRNAs not only serve as non-coding regulators but also have the capacity to encode biologically active peptides. Compared with noncancerous cells, cancer cells have greater iron requirements, and ferroptosis occurs in response to radiotherapy, chemotherapy, and immunotherapy; therefore, ferroptosis activation may be a potential strategy to overcome the shortcomings of conventional cancer therapy.
methodsA mouse model of ferroptosis in gastric cancer was constructed, and a bioinformatics analysis was performed to analyze and characterize the circRNAs involved in ferroptosis in gastric cancer. The inhibitory effect of hsa_circ_0002301 on ferroptosis in tumors was confirmed both in vitro and in vivo. The presence and expression of HECTD1-463aa were verified using mass spectrometry, protein blotting, and immunofluorescence staining. The molecular mechanism of hsa_circ_0002301 was investigated using mass spectrometry and immunoprecipitation.
resultsWe designed and synthesized antibodies specific for the small protein HECTD1-463aa encoded by hsa_circ_0002301 to verify its presence and purified HECTD1-463aa by constructing hsa_circ_0002301 overexpression vectors with FLAG tags and used liquid chromatography-tandem mass spectrometry (LC‒MS/MS) to detect the characterized peptides. In addition, HECTD1 binding to HECTD1-463aa was identified by immunoprecipitation (Co-IP) and mass spectrometry. We found that HECTD1-463aa inhibited HECTD1-mediated GPX4 ubiquitination by binding to HECTD1, an important regulator of cell death in ferroptotic cancer cells.
conclusionshsa_circ_0002301 competitively inhibits the degradation of the GPX4 protein by HECTD1 through the encoded proteins HECTD1-463aa and HECTD1 to affect the ferroptosis level in gastric cancer cells.
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.