ArticleJournal of translational medicine2024
Identification of TEFM as a potential therapeutic target for LUAD treatment.
Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- SIRT5-dependent desuccinylation licenses UBR5-mediated degradation of TAMM41 to regulate mitochondrial metabolism in lung adenocarcinoma.Biology direct · 2026Article
- Dacomitinib in Combination with chemotherapy is effective in lung adenocarcinoma with rareFrontiers in oncology · 2026Article
- Guanylate-binding proteins score and a CBFA2T3-included risk model define immune microenvironment and chemosensitivity in lung adenocarcinoma.European journal of medical research · 2025Article
- SLC25A39 overexpression exacerbates lung adenocarcinoma progression and is negatively regulated by AFG3L2.NPJ precision oncology · 2025Article
- Mitochondria-related gene-based molecular subtypes of lung adenocarcinoma and their prognostic implications.Scientific reports · 2025Article
- ADRB2 is regulated by TRIM22 and facilitates lung adenocarcinoma progression via JAK2/STAT3 signaling pathway.Scientific reports · 2025Article
- Integration of multi-omics and single-cell transcriptome reveals mitochondrial outer membrane protein-2 (MTX-2) as a prognostic biomarker and characterizes ubiquinone metabolism in lung adenocarcinoma.Journal of Cancer · 2025Article
- TEFM facilitates uterine corpus endometrial carcinoma progression by activating ROS-NFκB pathway.Journal of translational medicine · 2024Article
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Authors and funding
10 authors.
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Abstract
backgroundMolecularly targeted therapies have recently become a hotspot in the treatment of LUAD, with ongoing efforts to identify new effective targets due to individual variability. Among these potential targets, the mitochondrial transcription elongation factor (TEFM) stands out as a crucial molecule involved in mitochondrial synthetic transcriptional processing. Dysregulation of TEFM has been implicated in the development of various diseases; however, its specific role in LUAD remains unclear.
methodsWe conducted a comprehensive analysis of TEFM expression in LUAD, leveraging data from the TCGA database. Subsequently, we validated these findings using clinical specimens obtained from the First Affiliated Hospital of Soochow University, employing western blotting and qRT-PCR techniques. Further experimental validation was performed through the transfection of cells with TEFM overexpression, knockdown, and knockout lentiviruses. The effects of TEFM on LUAD were evaluated both in vitro and in vivo using a range of assays, including CCK-8, colony formation, EdU incorporation, Transwell migration, Tunel assay, flow cytometry, JC-1 staining, and xenograft tumour models.
resultsOur investigation uncovered that TEFM exhibited elevated expression levels in LUAD and exhibited co-localization with mitochondria. Overexpression of TEFM facilitated malignant processes in LUAD cells, whereas its silencing notably curbed these behaviors and induced mitochondrial depolarization, along with ROS production, culminating in apoptosis. Moreover, the absence of TEFM substantially influenced the expression of mitochondrial transcripts and respiratory chain complexes. Results from nude mouse xenograft tumors further validated that inhibiting TEFM expression markedly hindered tumor growth.
conclusionTEFM promotes LUAD malignant progression through the EMT pathway and determines apoptosis by affecting the expression of mitochondrial transcripts and respiratory chain complexes, providing a new therapeutic direction for LUAD-targeted therapy.
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