ArticleCancer cell international2025
Co-delivery of camptothecin and SH3RF3-AS1 SiRNA for glioma synergistic therapy.
Article in Cancer cell international, 2025. 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
9 authors.
Funding
Abstract
backgroundCurrent treatment strategies for high-grade gliomas have a limited overall patient benefit. Here, Methylated RNA immunoprecipitation sequencing (MeRIP-seq) of glioma was conducted to screen the lncRNA regulated by m6A modification in glioma, and provide an innovative chemotherapeutic strategy to improved the therapeutic efficacy.
methodsTo elucidate the impact and the molecular mechanism of ALKBH5/SH3RF3-AS1/SH3RF3 regulation on glioma malignancy, proliferation phenotypic assays, MeRIP-qPCR, RIP-qPCR and western blotting were used. Expressions and clinical significances of ALKBH5, SH3RF3-AS1, and SH3RF3 were assessed in tissue chip. Furthermore, we designed a nanodrug (Nano
resultsSH3RF3-AS1 was demethylated and overexpressed in glioma. We elucidated the mechanistic link between ALKBH5-mediated N6-methyladenosine (m6A) modification and SH3RF3-AS1 expression, and the cis-regulation of SH3RF3-AS1 to SH3RF3. Clinically, the ALKBH5, SH3RF3-AS1, and SH3RF3 expression increased with increasing glioma grade, high SH3RF3-AS1 expression correlated with unfavorable 5-year overall survival and progression-free survival in a cohort of 148 glioma patients. SH3RF3-AS1 drived glioma progression and promoted chemoresistance to camptothecin (CPT). We designed a nanodrug (Nano
conclusionOur findings provide valuable insights into the roles of m6A demethylation-mediated upregulation of SH3RF3-AS1 in supporting glioma proliferation and demonstrate the potential of Nano
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.