ArticleTranslational oncology2026
Molecular mechanisms and therapeutic targeting implications of ER/mTOR signaling axis-driven tumor progression in aggressive meningiomas.
Article in Translational oncology, 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
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeAggressive meningiomas pose substantial clinical challenges because of their high rates of recurrence. The aim of this study is to investigate the mechanistic role of estrogen receptor (ER)-mediated mTOR hyperactivation in promoting meningioma progression and to evaluate the therapeutic potential of targeting this signaling axis with tamoxifen.
methodsAnalyses involving data from clinical registries have established sex as a predictor of adverse outcomes, while multiomics investigations have revealed the overexpression of ER in advanced-grade and recurrent tumors. Functional validation was conducted using ER knockdown models. Mechanistic insights were obtained through RNA sequencing, with orthogonal validation performed via qPCR and Western blotting, with a focus on regulators of the mTOR pathway (RICTOR, PIK3CA, and DEPTOR). Therapeutic efficacy was evaluated in meningioma cell models through pharmacological inhibition using tamoxifen.
resultsClinical analysis was used to identify sex as a predictor of adverse outcomes, revealing that ER overexpression is significantly correlated with advanced tumor grades. Silencing of the ER markedly reduced malignant phenotypes, leading to decreased cell proliferation and invasion, while also inducing apoptosis. Mechanistically, ER activation resulted in the upregulation of RICTOR and PIK3CA expression, alongside suppression of DEPTOR, which directly activated mTOR signaling. Tamoxifen exhibited potent antitumor effects by reversing this oncogenic signaling cascade.
conclusionThis study revealed that the ER/mTOR axis is associated with sex-linked therapeutic vulnerability in aggressive meningiomas. This finding provides mechanistic evidence for ER-driven mTOR activation via the dysregulation of RICTOR/PIK3CA-DEPTOR. The demonstrated efficacy of tamoxifen supports its clinical repurposing as a targeted therapy for ER-positive meningiomas, offering a biologically rational strategy to address therapeutic resistance in this challenging malignancy.
Indexed as
Identifiers
What Socratic 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 Socratic graph.