TET1-mediated DNA demethylation and transcription activation of MRPS17 induces lung adenocarcinoma through PI3K-AKT-mTOR pathway.
What this study shows
TET1 demethylates the MRPS17 promoter to drive MRPS17 overexpression in lung adenocarcinoma, activating PI3K-AKT-mTOR signalling and increasing proliferation, migration and invasion. MRPS17 knockdown induces apoptosis and suppresses tumour growth in vitro and in vivo.
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Human LUAD cell lines; mouse xenograft) rather than a whole-organism health-outcome study. That is often exactly where causal biology gets established -- the code says which system the finding was shown in, and nothing about how good the work is. |
| Study type | 5 - Mechanistic / In Vitro |
| Model system | Human LUAD cell lines; mouse xenograft |
| Journal | Journal of Molecular Histology |
| Year | 2026 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1007/s10735-026-10862-8 · PMID 42665721 · Free full text (PMC13525032) |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | MRPS17 overexpression / knockdown; TET1 modulation |
| Target | MRPS17; TET1; PI3K-AKT-mTOR |
| Model | Human cell lines; mouse xenograft |
| Effect | MRPS17 upregulation activates PI3K-AKT-mTOR and increases tumour aggressiveness; knockdown induces apoptosis and reduces tumour growth |
In the Atlas
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