ArticleCell death & disease2021
Elevated TEFM expression promotes growth and metastasis through activation of ROS/ERK signaling in hepatocellular carcinoma.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- The distinct roles of ROS in tumor immunity: from mechanisms to immunotherapeutic applications.Journal of hematology & oncology · 2026Review
- Circulating microRNAs as Biomarkers of Brain Metastases in Lung Cancer: A Pilot Study.Journal of clinical medicine · 2026Article
- Expressional and prognostic value of cytokine receptor-like factor 3 in liver hepatocellular carcinoma patients via integrated bioinformatics analyses and experiments.SAGE open medicine · 2026Article
- Erk1/2 Orchestrates SSPH I-Induced Oxidative Stress, Mitochondrial Dysfunction and Ferroptosis in Hepatocellular Carcinoma.Journal of cellular and molecular medicine · 2025Article
- Mitochondrial Reactive Oxygen Species (mROS) Generation and Cancer:International journal of nanomedicine · 2025Review
- TEFM facilitates uterine corpus endometrial carcinoma progression by activating ROS-NFκB pathway.Journal of translational medicine · 2024Article
- Mitochondrial transcription elongation factor TEFM promotes malignant progression of gliomas.Cancer cell international · 2024Article
- Exploring potential causal genetic variants and genes for endometrial cancer: Open Targets Genetics, Mendelian randomization, and multi-tissue transcriptome-wide association analysis.Translational cancer research · 2024Article
- Mitochondria: a new intervention target for tumor invasion and metastasis.Molecular medicine (Cambridge, Mass.) · 2024Review
- Review
- Identification of TEFM as a potential therapeutic target for LUAD treatment.Journal of translational medicine · 2024Article
- Cell-specific modulation of mitochondrial respiration and metabolism by the pro-apoptotic Bcl-2 family members Bax and Bak.Apoptosis : an international journal on programmed cell death · 2024Article
- SB431542 partially inhibits high glucose-induced EMT by restoring mitochondrial homeostasis in RPE cells.Cell communication and signaling : CCS · 2024Article
- LC-MS/MS analysis reveals plasma protein signatures associated with lymph node metastasis in colorectal cancer.Frontiers in immunology · 2024Article
- Ribonucleotide synthesis by NME6 fuels mitochondrial gene expression.The EMBO journal · 2023Article
- MAPK/ERK Pathway as a Central Regulator in Vertebrate Organ Regeneration.International journal of molecular sciences · 2022Review
- The Role of MIEF2 in Cisplatin Sensitivity in KIRP Patients: Insights from Four-gene Mitochondrial Fusion RNA Markers.Technology in cancer research & treatmentArticle
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TEFM (transcription elongation factor of mitochondria) has been identified as a novel nuclear-encoded transcription elongation factor in the transcription of mitochondrial genome. Our bioinformatics analysis of TCGA data revealed an aberrant over-expression of TEFM in hepatocellular carcinoma (HCC). We analyzed its biological effects and clinical significance in this malignancy. TEFM expression was analyzed by quantitative real-time PCR, western blot, and immunohistochemistry analysis in HCC tissues and cell lines. The effects of TEFM on HCC cell growth and metastasis were determined by cell proliferation, colony formation, flow cytometric cell cycle and apoptosis, migration, and invasion assays. TEFM expression was significantly increased in HCC tissues mainly caused by down-regulation of miR-194-5p. Its increased expression is correlated with poor prognosis of HCC patients. TEFM promoted HCC growth and metastasis both in vitro and in vivo by promoting G1-S cell transition, epithelial-to-mesenchymal transition (EMT), and suppressing cell apoptosis. Mechanistically, TEFM exerts its tumor growth and metastasis promoting effects at least partly through increasing ROS production and subsequently by activation of ERK signaling. Our study suggests that TEFM functions as a vital oncogene in promoting growth and metastasis in HCC and may contribute to the targeted therapy of HCC.
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