ArticleFrontiers in pharmacology2026
Niraparib promotes ferroptosis by inhibiting TM4SF1 expression through ALKBH1-mediated 6mA modification in BRCA wild-type ovarian cancer.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Niraparib significantly improves the prognosis of patients with BRCA wild-type ovarian cancer (BRCAwt OC). However, the underlying mechanisms remain elusive. N6-methyladenine DNA (6mA) modification has emerged as a critical epigenetic regulator in cancer progression. We investigated whether niraparib exerts antitumor effects by modulating 6mA modification in BRCAwt OC models. Methods: The 6mA modification levels were assessed using dot blot, ELISA, and 6mA-IP-seq. The regulatory role of ALKBH1 in transmembrane 4 L six family member 1 (TM4SF1) mRNA expression and 6mA modification was examined via RT-qPCR, Western blot, and 6mA-IP-qPCR, respectively. Using the CCK-8 assay, colony formation assay, wound healing assay, Transwell assay, and subcutaneous tumor xenograft models, the function of TM4SF1 in tumor growth was evaluated Results: Our findings demonstrated that niraparib treatment significantly reduced the expression of TM4SF1 by increasing ALKBH1-mediated 6mA modification. Mechanistically, niraparib increases the expression of ALKBH1, which binds to the TM4SF1 promoter, thereby regulating its 6mA modification and suppressing its expression. Furthermore, TM4SF1 knockdown reduced cell proliferation, invasion, and migration, along with tumor growth Conclusion: Niraparib exhibits antitumor effects and promotes ferroptosis by inhibiting TM4SF1 expression through ALKBH1-mediated 6mA modification in BRCAwt OC. These findings emphasize the potential application of niraparib in BRCAwt OC and reveal the important role of epigenetic regulation in cancer treatment.
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.