ArticleFrontiers in genetics2025
FEZF1-AS1 drives autophagy-mediated progression of colon cancer and reduces chemosensitivity through inhabiting the PI3K/AKT/mTOR signaling pathway.
Article in Frontiers in genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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.
- LncSMIM14 Hijacks Rab3a-Mediated Endocytosis to Promote Bovine Viral Diarrhea Virus Replication.International journal of molecular sciences · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis and chemoresistance mechanisms of colon cancer (CC) are still unclear. Here, we find that a long non-coding RNA (lncRNA), FEZ family zinc finger 1-antisense RNA 1 (FEZF1-AS1), is highly expressed in CC, which may be caused by the amplification mutation of FEZF1-AS1 at the gene level through bioinformatic analysis. FEZF1-AS1 has the potential to be a biomarker in the diagnosis of CC. Functionally, FEZF1-AS1 promotes the proliferation, invasion, metastasis, and survival of CC cells and reduces the sensitivity of CC cells to oxaliplatin. Mechanistically, FEZF1-AS1 drives autophagy-mediated development of CC and reduces chemosensitivity to oxaliplatin through inhabiting the PI3K/AKT/mTOR signaling pathway. In summary, our data suggest that FEZF1-AS1 may be a key driver of CC progression and chemotherapy resistance, and targeting FEZF1-AS1 may be a potential strategy for the diagnosis and treatment of CC.
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.