ArticlePloS one2025
ETS2 targets ZMYND11 to inhibit thyroid cancer progression via the mTOR signaling pathway.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDespite advancements in thyroid cancer (THCA) treatment, the prognosis for advanced cases remains poor. Cellular senescence is crucial in tumor progression, with ETS2 emerging as a key regulator. However, the role of ETS2 and its interaction with ZMYND11 in THCA is unclear.
methodsDifferentially expressed genes (DEGs) connected with cellular senescence were determined from The Cancer Genome Atlas (TCGA)-THCA dataset. Functional analysis, prognostic risk model, and nomogram were then performed to identify ETS2 as a hub gene. The roles of ETS2 and ZMYND11 were explored using Western blotting (WB), co-immunoprecipitation (Co-IP), and quantitative real-time polymerase chain reaction (qRT-PCR). Effects of ETS2 overexpression and knockdown of ZMYND11 on apoptosis, cell proliferation, epithelial-mesenchymal transition (EMT), and mTOR signaling were evaluated. In vivo, a xenograft model was established using Cal-62 cells with or without ETS2 overexpression to assess tumor growth and protein expression.
resultsETS2 was notably downregulated in THCA, and its low expression was connected to adverse prognosis. ETS2 overexpression inhibited THCA cell invasion, migration, proliferation, and induced apoptosis. ETS2 also regulated the expression of EMT markers, indicating its role in inhibiting THCA progression. Co-IP analysis showed that ETS2 interacted with ZMYND11. Knockdown of ZMYND11 attenuated the inhibitory effect of ETS2 on THCA cell behavior and mTOR pathway regulation. In vivo, ETS2 overexpression reduced tumor growth and increased ETS2 and ZMYND11 expression in xenograft tumors.
conclusionThis study identified the cellular senescence gene ETS2 as a tumor suppressor in THCA, which interacts with ZMYND11 to regulate THCA tumor progression through the mTOR pathway, thereby inhibiting cell senescence. Targeting the ETS2-ZMYND1 axis may provide new therapeutic strategies and prognostic biomarkers for THCA.
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.