ArticleJournal of experimental & clinical cancer research : CR2026
Targeting FAM83D triggers tumor cell senescence via cGAS-STING signaling activation and reprograms TAMs to combat glioma.
Article in Journal of experimental & clinical cancer research : CR, 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
13 authors.
Funding
Abstract
backgroundGlioma, a prevalent and aggressive primary brain tumor, has a poor prognosis despite the administration of standard treatment. Cellular senescence is thought to have a good protective effect in limiting the malignant progression of tumors, while the senescence-associated secretory phenotype produced by senescent cells may influence the activity of immune cells in the microenvironment. Macrophages, as a major component of the glioma microenvironment, play an important role in regulating the innate and adaptive immune responses which is essential for tumor suppression. Therefore, identifying potential targets that connect tumor cell senescence with macrophage reprogramming may facilitate the development of new therapeutic agents in glioma.
methodsHere, we developed the CellToAge algorithm and leveraged high-throughput sequencing data to map senescence-associated signatures in glioma. Based on in vitro and in vivo experiments including the cell co-culture model, in situ allograft mouse model, and single-cell transcriptome sequencing, we further elucidated the interplay between tumor cell senescence and macrophage polarization induced by knockdown of FAM83D in glioma.
resultsNotably, we identified the projected senescence-associated signatures in glioma (PSAG) and focused on the potential target FAM83D. In vitro and in vivo assays showed that knockdown of FAM83D resulted in abnormal cell division, which increased double-stranded DNA in the cytoplasm, thereby inducing tumor cell senescence by activating the cGAS-STING signaling to suppress glioma progression. Synchronously, knockdown of FAM83D could also induce glioma cells to produce a specific senescence-associated secretory phenotype (SASP), which promoted the senescence of neighboring tumor cells and drove macrophage polarization toward an M1 state. Additionally, ANXA1-FPR1/2 ligand-receptor signaling involved in tumor cells-macrophages crosstalk was associated with macrophage polarizations, which was further validated based on our clinical glioma cohort.
conclusionsOur data revealed the critical role of FAM83D in regulating tumor cell senescence and shaping the tumor microenvironment with a specific impact on macrophage polarization. These insights open avenues for targeted therapeutic strategies aimed at modulating the FAM83D-cGAS/STING-SASP-TAMs axis in the management of glioma.
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.