ArticleJournal of translational medicine2026
The MAFG-AS1/G6PD axis reduces platinum sensitivity in colorectal cancer through pentose phosphate pathway activation.
Article in Journal of translational medicine, 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
9 authors.
Funding
Abstract
backgroundChemoresistance remains a major challenge in colorectal cancer (CRC) treatment. Metabolic reprogramming is a cancer hallmark, with the pentose phosphate pathway (PPP) playing a ceral role. This study aimed to investigate the role of the long noncoding RNA MAFG-AS1 in CRC chemoresistance and its underlying mechanism.
methodsMAFG-AS1 expression was analyzed using TCGA data. Functional roles were assessed via RNA interference, overexpression, RNA pull-down, RIP, metabolic flux analysis, isotope tracing, and xenograft models, combined with qPCR, Western blot, flow cytometry, and IHC. Statistical analyses used t-tests and ANOVA.
resultsMAFG-AS1 was upregulated in CRC, driven transcriptionally by c-Myc. It directly bound to and stabilized G6PD homodimers, enhancing its enzymatic activity. This activated the PPP, increased NADPH production, reduced ROS levels, maintained redox homeostasis, and promoted CRC cell proliferation and tumor growth. MAFG-AS1 knockdown sensitized CRC cells to cisplatin and oxaliplatin.
conclusionMAFG-AS1 promotes metabolic reprogramming and reduces platinum sensitivity in CRC by enhancing G6PD-dependent PPP flux and redox buffering capacity. Targeting the MAFG-AS1–G6PD axis may represent a potential strategy to improve the efficacy of platinum-based chemotherapy.
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.