ArticleCell death & disease2023
HOXC13-driven TIMM13 overexpression promotes osteosarcoma cell growth.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Galactokinase 1 Positively Regulates Mitochondrial Respiration by Phosphorylating TIMM13 as a Protein Kinase.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Ubiquitin-conjugating enzyme UBE2N modulates proteostasis in immunoproteasome-positive acute myeloid leukemia.The Journal of clinical investigation · 2025Article
- An immunotherapy guide constructed by cGAS-STING signature for breast cancer and the biofunction validation of the pivotal gene HOXC13 viaFrontiers in immunology · 2025Article
- DDX49 as a novel prognostic biomarker regulates colorectal cancer cell proliferation through the TIMM44-PI3K-AKT pathway.Frontiers in oncology · 2025Article
- TIMM8A-TIMM13 Complex Exerts Oncogenic Functions in Lung Cancer.Oncology research · 2025Article
- Targeting POLRMT by IMT1 inhibits colorectal cancer cell growth.Cell death & disease · 2024Article
- Xenografting Human Musculoskeletal Sarcomas in Mice, Chick Embryo, and Zebrafish: How to Boost Translational Research.Biomedicines · 2024Review
- UBXN1 promotes liver tumorigenesis by regulating mitochondrial homeostasis.Journal of translational medicine · 2024Article
- Lipid Peroxidation-Related Redox Signaling in Osteosarcoma.International journal of molecular sciences · 2024Review
- A first-in-class TIMM44 blocker inhibits bladder cancer cell growth.Cell death & disease · 2024Article
- Targeting POLRMT by a first-in-class inhibitor IMT1 inhibits osteosarcoma cell growth in vitro and in vivo.Cell death & disease · 2024Article
- The Genetic Selection ofAnimals : an open access journal from MDPI · 2024Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TIMM13 (translocase of inner mitochondrial membrane 13) located at the mitochondrial intermembrane space is vital for the integrity and function of mitochondria. We found that the mitochondrial protein TIMM13 is upregulated in human OS tissues and cells. In patient-derived primary OS cells and established cell lines, TIMM13 shRNA or knockout provoked mitochondrial dysfunction, causing mitochondrial depolarization, reactive oxygen species production, and oxidative injury, as well as lipid peroxidation, DNA damage, and ATP depletion. Moreover, TIMM13 depletion provoked OS cell apoptosis and inhibited cell proliferation and migration. Conversely, ectopic TIMM13 overexpression increased ATP contents, enhancing OS cell proliferation and migration. Moreover, we discovered that Akt-mTOR activation was inhibited with TIMM13 depletion in primary OS cells. Further studies revealed that HOXC13 (Homeobox C13)-dependent TIMM13 transcription was significantly increased in OS tissues and cells. Whereas TIMM13 transcription and expression were decreased following HOXC13 silencing in primary OS cells. In vivo, TIMM13 KO potently inhibited OS xenograft growth in the proximal tibia of nude mice. TIMM13 KO also induced Akt-mTOR inactivation, ATP depletion, oxidative injury, and apoptosis in the in situ OS tumors. Together, upregulation of the mitochondrial protein TIMM13 is important for OS cell growth, representing a novel and promising therapeutic target.
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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 Socratic graph.