---
title: "TET1-driven demethylation of MRPS17 promotes LUAD via the PI3K-AKT-mTOR pathway"
id: "pubmed-42665721"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42665721"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42665721/"
doi: "10.1007/s10735-026-10862-8"
published_at: "2026-08-29T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# TET1-driven demethylation of MRPS17 promotes LUAD via the PI3K-AKT-mTOR pathway
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42665721
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42665721/)
- **DOI:** [10.1007/s10735-026-10862-8](https://doi.org/10.1007%2Fs10735-026-10862-8)
- **Published At:** 2026-08-29T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- The study investigates the role of mitochondrial ribosomal protein S17 (**MRPS17**) in lung adenocarcinoma (**LUAD**) and its regulation by the DNA demethylase **TET1**. - Analysis of LUAD tissues showed **MRPS17** upregulation and an association with worse prognosis in patients. - Functional experiments in LUAD cell lines demonstrated that **MRPS17** overexpression enhances proliferation, migration, and invasion, while **MRPS17** knockdown increases apoptosis and reduces tumorigenic properties in vitro and in vivo. - Epigenetic assays identified **TET1** as a regulator that demethylates the **MRPS17** promoter, increasing MRPS17 transcription. - Activation of the **PI3K-AKT-mTOR** signaling cascade was observed downstream of MRPS17, implicating this pathway in MRPS17-driven tumor aggressiveness. - The authors propose a mechanistic axis: **TET1**-mediated promoter demethylation → increased **MRPS17** expression → activation of **PI3K-AKT-mTOR** → enhanced LUAD progression. - The study positions **MRPS17** as a potential prognostic biomarker and a candidate therapeutic target, and it highlights epigenetic modulation of MRPS17 as a possible intervention point. - Details such as cohort size, specific experimental conditions, quantitative effect sizes, and some methodological specifics were not reported in the PubMed abstract and would require consulting the full article for verification. - Ethical approvals for retrospective human data use and animal experiments were obtained from Harbin Medical University Cancer Hospital; informed consent was waived for retrospective samples and data were anonymized. - Authors declared no conflicts of interest.
## Clinical Analysis & Structured Key Points
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Affiliations Expand ### Affiliations * 1 Department of Oncology, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang District, Heilongjiang, 150001, Harbin, China. * 2 Department of Respiratory Oncology, Harbin Medical University Cancer Hospital, 150 Haping Road, Nangang District, Harbin, 150040, Heilongjiang Province, China. * 3 Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, 150040, Heilongjiang Province, China. * 4 Department of cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, 150001, Heilongjiang Province, China. * 5 Surgical Department of Gynecologic Oncology, Harbin Medical University Cancer Hospital, Harbin, 150040, Heilongjiang Province, China. * 6 Department of Respiratory Oncology, Harbin Medical University Cancer Hospital, 150 Haping Road, Nangang District, Harbin, 150040, Heilongjiang Province, China. 602135@hrbmu.edu.cn. * PMID: **42665721** * DOI: [ 10.1007/s10735-026-10862-8 ](https://doi.org/10.1007/s10735-026-10862-8) Item in Clipboard # TET1-mediated DNA demethylation and transcription activation of MRPS17 induces lung adenocarcinoma through PI3K-AKT-mTOR pathway Nan Zhou et al. J Mol Histol. 2026. Show details Display options Display options Format Abstract PubMed PMID J Mol Histol Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22J+Mol+Histol%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22J+Mol+Histol%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42665721/) . 2026 Aug 29;57(5):283. doi: 10.1007/s10735-026-10862-8. ### Authors [Nan Zhou](https://pubmed.ncbi.nlm.nih.gov/?term=Zhou+N&cauthor_id=42665721)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42665721/#short-view-affiliation-1 "Department of Oncology, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang District, Heilongjiang, 150001, Harbin, China.")[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42665721/#short-view-affiliation-2 "Department of Respiratory Oncology, Harbin Medical University Cancer Hospital, 150 Haping Road, Nangang District, Harbin, 150040, Heilongjiang Province, China."), [Lei Song](https://pubmed.ncbi.nlm.nih.gov/?term=Song+L&cauthor_id=42665721)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42665721/#short-view-affiliation-2 "Department of Respiratory Oncology, Harbin Medical University Cancer Hospital, 150 Haping Road, Nangang District, Harbin, 150040, Heilongjiang Province, China."), [Yang Wu](https://pubmed.ncbi.nlm.nih.gov/?term=Wu+Y&cauthor_id=42665721)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42665721/#short-view-affiliation-3 "Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, 150040, Heilongjiang Province, China."), [Ying Wei](https://pubmed.ncbi.nlm.nih.gov/?term=Wei+Y&cauthor_id=42665721)[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42665721/#short-view-affiliation-4 "Department of cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, 150001, Heilongjiang Province, China."), [Wenwen Zhang](https://pubmed.ncbi.nlm.nih.gov/?term=Zhang+W&cauthor_id=42665721)[ 5 ](https://pubmed.ncbi.nlm.nih.gov/42665721/#short-view-affiliation-5 "Surgical Department of Gynecologic Oncology, Harbin Medical University Cancer Hospital, Harbin, 150040, Heilongjiang Province, China."), [Bingbing Wang](https://pubmed.ncbi.nlm.nih.gov/?term=Wang+B&cauthor_id=42665721)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42665721/#short-view-affiliation-2 "Department of Respiratory Oncology, Harbin Medical University Cancer Hospital, 150 Haping Road, Nangang District, Harbin, 150040, Heilongjiang Province, China."), [Yanbin Zhao](https://pubmed.ncbi.nlm.nih.gov/?term=Zhao+Y&cauthor_id=42665721)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42665721/#short-view-affiliation-2 "Department of Respiratory Oncology, Harbin Medical University Cancer Hospital, 150 Haping Road, Nangang District, Harbin, 150040, Heilongjiang Province, China."), [Yan Wang](https://pubmed.ncbi.nlm.nih.gov/?term=Wang+Y&cauthor_id=42665721)[ 6 ](https://pubmed.ncbi.nlm.nih.gov/42665721/#short-view-affiliation-6 "Department of Respiratory Oncology, Harbin Medical University Cancer Hospital, 150 Haping Road, Nangang District, Harbin, 150040, Heilongjiang Province, China. 602135@hrbmu.edu.cn.") ### Affiliations * 1 Department of Oncology, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang District, Heilongjiang, 150001, Harbin, China. * 2 Department of Respiratory Oncology, Harbin Medical University Cancer Hospital, 150 Haping Road, Nangang District, Harbin, 150040, Heilongjiang Province, China. * 3 Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, 150040, Heilongjiang Province, China. * 4 Department of cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, 150001, Heilongjiang Province, China. * 5 Surgical Department of Gynecologic Oncology, Harbin Medical University Cancer Hospital, Harbin, 150040, Heilongjiang Province, China. * 6 Department of Respiratory Oncology, Harbin Medical University Cancer Hospital, 150 Haping Road, Nangang District, Harbin, 150040, Heilongjiang Province, China. 602135@hrbmu.edu.cn. * PMID: **42665721** * DOI: [ 10.1007/s10735-026-10862-8 ](https://doi.org/10.1007/s10735-026-10862-8) Item in Clipboard Cite Display options Display options Format Abstract PubMed PMID ## Abstract Lung adenocarcinoma (LUAD), characterized by its complex molecular heterogeneity and resistance to both conventional and targeted therapies, poses significant therapeutic challenges. Therefore, the identification of novel molecular targets is crucial for enhancing therapeutic strategies and improving patient outcomes. This study investigates the role of mitochondrial ribosomal protein S17 (MRPS17) in the progression of LUAD, with a specific focus on its interaction with the PI3K-AKT-mTOR signaling pathway. We conducted functional assays to assess cell proliferation, migration, invasion, and apoptosis in MRPS17-manipulated LUAD cell lines. Further, we explored the epigenetic regulation by TET1 through methylation analysis and investigated the downstream effects on the PI3K-AKT-mTOR pathway using Western blotting and reporter assays. Analysis revealed that MRPS17 is upregulated in LUAD tissues and is associated with a poor prognosis. In cellular models, MRPS17 overexpression was shown to promote proliferation, migration, and invasion, whereas its knockdown induced apoptosis and diminished tumorigenic capabilities both in vitro and in vivo. Importantly, TET1 was identified as a crucial regulator of MRPS17, acting through the demethylation of its promoter to enhance MRPS17 expression and subsequently activate the PI3K-AKT-mTOR pathway. MRPS17 significantly contributes to LUAD progression by enhancing tumor aggressiveness through the PI3K-AKT-mTOR pathway. The TET1-mediated demethylation of MRPS17 introduces a novel epigenetic mechanism that could be leveraged for targeted therapeutic interventions. This study not only provides foundational insights into the molecular biology of LUAD but also highlights the potential of MRPS17 as a prognostic marker and therapeutic target. **Keywords:** LUAD; MRPS17; PI3K-AKT-mTOR. © 2026. The Author(s). [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement Declarations. Conflict of interest: The authors declare that they have no conflicts of interest. Ethical approval: This retrospective study and the animal experiments were approved by the Medical Ethics Committee of Harbin Medical University Cancer Hospital and were conducted in accordance with established Human welfare guidelines (2021-27-IIT) and established animal welfare guidelines(KY2022-54). Informed consent: Considering the retrospective nature of the study, informed consent was waived. The data used in this study were anonymized before use. ## References 1. 1. Alnafakh R, Saretzki G, Midgley A, Flynn J, Kamal AM, Dobson L et al (2021) Aberrant Dyskerin expression is related to proliferation and poor survival in endometrial cancer. Cancers (Basel) 13(2):273 - [PubMed](https://pubmed.ncbi.nlm.nih.gov/33450922/) - [PMC](https://pmc.ncbi.nlm.nih.gov/articles/7828388/) 2. 1. Alrehaili AA, Gharib AF, Alghamdi SA, Alhazmi A, Al-Shehri SS, Hagag HM et al (2023) Evaluation of TET family gene expression and 5-hydroxymethylcytosine as potential epigenetic markers in non-small cell lung cancer. Vivo 37(1):445–453 3. 1. Baughman JM, Nilsson R, Gohil VM, Arlow DH, Gauhar Z, Mootha VK (2009) A computational screen for regulators of oxidative phosphorylation implicates SLIRP in mitochondrial RNA homeostasis. PLoS Genet 5(8):e1000590 - [PubMed](https://pubmed.ncbi.nlm.nih.gov/19680543/) - [PMC](https://pmc.ncbi.nlm.nih.gov/articles/2721412/) 4. 1. Chen J, Alduais Y, Zhang K, Zhu X, Chen B (2021) CCAT1/FABP5 promotes tumour progression through mediating fatty acid metabolism and stabilizing PI3K/AKT/mTOR signalling in lung adenocarcinoma. J Cell Mol Med 25(19):9199–9213 - [PubMed](https://pubmed.ncbi.nlm.nih.gov/34431227/) - [PMC](https://pmc.ncbi.nlm.nih.gov/articles/8500980/) 5. 1. Chen P, Quan Z, Song X, Gao Z, Yuan K (2022) MDFI is a novel biomarker for poor prognosis in LUAD. Front Oncol 12:1005962 - [PubMed](https://pubmed.ncbi.nlm.nih.gov/36300089/) - [PMC](https://pmc.ncbi.nlm.nih.gov/articles/9589366/) Show all 52 references ## MeSH terms * Adenocarcinoma of Lung* / genetics Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Adenocarcinoma+of+Lung%2Fgenetics%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Adenocarcinoma+of+Lung) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42665721/) * Adenocarcinoma of Lung* / metabolism Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Adenocarcinoma+of+Lung%2Fmetabolism%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Adenocarcinoma+of+Lung) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42665721/) * Adenocarcinoma of Lung* / pathology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Adenocarcinoma+of+Lung%2Fpathology%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Adenocarcinoma+of+Lung) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42665721/) * Animals Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Animals%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Animals) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42665721/) * Apoptosis / genetics Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Apoptosis%2Fgenetics%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nl
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