ArticleCell communication and signaling : CCS2026
Loss of cold shock domain-containing protein E1 (CSDE1) function enhances mRNA stability of interleukin-6 and promotes malignant transformation in endometrial cancer cells.
Article in Cell communication and signaling : CCS, 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
11 authors.
Funding
Abstract
backgroundRNA-binding proteins (RBPs) are indispensable effectors of post-transcriptional gene regulation and are increasingly recognized as pivotal modulators of oncogenic signaling pathways. Cold shock domain-containing protein E1 (CSDE1) has been reported to be dysregulated or mutated in several malignancies; however, its functional significance and the mechanistic basis of its involvement in endometrial cancer (EC) progression remain poorly understood.
methodsBioinformatic analysis of The Cancer Genome Atlas (TCGA) was employed to characterize CSDE1 expression and mutation profiles in EC. CRISPR/Cas9-mediated knockout (KO) was used to establish CSDE1-deficient EC cell lines. The impact on cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) was evaluated through standard functional assays. To identify downstream targets, transcriptomic profiling was integrated with RNA-protein interaction assay and mRNA stability analysis. Finally, functional rescue experiments were conducted using shRNA-mediated IL-6 silencing and pharmacological inhibition with the IL-6 antagonist Siltuximab.
resultsCSDE1 is frequently mutated and significantly downregulated in EC tissues compared to normal controls. Loss of CSDE1 markedly accelerated EC cell proliferation, migration, invasion, and the acquisition of EMT-associated phenotypes. Transcriptomic analysis identified IL-6 as a prominent downstream target that is significantly upregulated upon CSDE1 depletion. Mechanistically, CSDE1 directly binds to IL-6 mRNA and negatively regulates its stability, thereby restraining IL-6 expression. Notably, both genetic silencing of IL-6 and pharmacological neutralization of IL-6 signaling with Siltuximab effectively abrogated the aggressive malignant phenotypes induced by CSDE1 loss.
conclusionsThese findings establish CSDE1 as a novel tumor suppressor in EC and elucidate a previously unrecognized post-transcriptional CSDE1-IL-6 regulatory axis. By linking RBP-mediated mRNA stability to oncogenic inflammatory signaling, our study provides critical insights into the molecular drivers of EC progression. Furthermore, we identify the IL-6 signaling pathway as a significant therapeutic vulnerability that could be exploited to treat CSDE1-deficient EC.
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.