ArticleCellular and molecular life sciences : CMLS2016
TUFM downregulation induces epithelial-mesenchymal transition and invasion in lung cancer cells via a mechanism involving AMPK-GSK3β signaling.
Article in Cellular and molecular life sciences : CMLS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 58 citations in OpenAlex.
- The dual role of AMPK in cancer metabolic reprogramming.Molecular biology reports · 2026Review
- TUFM: a central regulator in mitochondrial quality control and beyond.Cell death discovery · 2026Review
- Pleiotropic regulation of mitochondrial translational factors in governing proliferation, apoptosis and metastasis during cancer progression.World journal of clinical oncology · 2026Review
- SIRT7 drives energy metabolic shifts in endometriosis via interaction with TUFM and Rhoa/Rock/Akt pathway activation.Cellular and molecular life sciences : CMLS · 2025Article
- A novel necroptosis related prognostic signature for skin cutaneous melanoma based on transcriptome and single cell sequencing analysis.Scientific reports · 2025Article
- Multi-omics analysis untangles the crosstalk between intratumor microbiome, lactic acid metabolism and immune status in lung squamous cell carcinoma.Frontiers in immunology · 2025Article
- Short-term regulation of TSFM level does not alter amyloidogenesis and mitochondrial function in type-specific cells.Molecular biology reports · 2024Article
- TUFM in health and disease: exploring its multifaceted roles.Frontiers in immunology · 2024Review
- Article
- Microwell-based flow culture increases viability and restores drug response in prostate cancer spheroids.Biotechnology journal · 2023Article
- Fumarate hydratase inhibits non-small cell lung cancer metastasis via inactivation of AMPK and upregulation of DAB2.Oncology letters · 2023Article
- FUNDC1 protects against doxorubicin-induced cardiomyocyte PANoptosis through stabilizing mtDNA via interaction with TUFM.Cell death & disease · 2022Article
- Effects of short-term waterfall forest aerosol air exposure on rat lung proteomics.Annals of translational medicine · 2022Article
- Silencing TUFM Inhibits Development of Monocrotaline-Induced Pulmonary Hypertension by Regulating Mitochondrial Autophagy via AMPK/mTOR Signal Pathway.Oxidative medicine and cellular longevity · 2022Article
- Bothrops Jararaca Snake Venom Modulates Key Cancer-Related Proteins in Breast Tumor Cell Lines.Toxins · 2021Article
- MicroRNA-217 inhibits the proliferation and invasion, and promotes apoptosis of non-small cell lung cancer cells by targeting sirtuin 1.Oncology letters · 2021Article
- Proteomic comparison between different tissue preservation methods for identification of promising biomarkers of urothelial bladder cancer.Scientific reports · 2021Article
- VSP‑17 suppresses the migration and invasion of triple‑negative breast cancer cells through inhibition of the EMT process via the PPARγ/AMPK signaling pathway.Oncology reports · 2021Article
- Article
- Prognostic Value and Related Regulatory Networks of MRPL15 in Non-Small-Cell Lung Cancer.Frontiers in oncology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction and epithelial-to-mesenchymal transition (EMT) play important roles in cancer development and metastasis. However, very little is known about the connection between mitochondrial dysfunction and EMT. Tu translation elongation factor, mitochondrial (TUFM), a key factor in the translational expression of mitochondrial DNA, plays an important role in the control of mitochondrial function. Here, we show that TUFM is downregulated in human cancer tissues. TUFM expression level was positively correlated with that of E-cadherin and decreased significantly during the progression of human lung cancer. TUFM knockdown induced EMT, reduced mitochondrial respiratory chain activity, and increased glycolytic function and the production of reactive oxygen species (ROS). Mechanistically, TUFM knockdown activated AMPK and phosphorylated GSK3β and increased the nuclear accumulation of β-catenin, leading to the induction of EMT and increased migration and metastasis of A549 lung cancer cells. Although TUFM knockdown also induced EMT of MCF7 breast cancer cells, the underlying mechanism appeared somewhat different from that in lung cancer cells. Our work identifies TUFM as a novel regulator of EMT and suggests a molecular link between mitochondrial dysfunction and EMT induction.
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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.