ArticleMolecular medicine (Cambridge, Mass.)2023
DYNLT1 promotes mitochondrial metabolism to fuel breast cancer development by inhibiting ubiquitination degradation of VDAC1.
Article in Molecular medicine (Cambridge, Mass.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 14 citations in OpenAlex.
- LncRNA CCAT1/miR-490-3p/VDAC1 Axis Promotes Colorectal Cancer Progression by Activating Glycolysis.Biochemical genetics · 2026Article
- Celastrol inhibits the DPYSL2-JAK/STAT pathway by targeting mito-IDHs mediated mitochondrial metabolism to exhaust breast cancer.Acta pharmacologica Sinica · 2025Article
- Autophagy-Related Proteins in Triple-Negative Breast Cancer: From Molecular Insights to Therapeutic Applications.International journal of molecular sciences · 2025Review
- Generation and characterization of a DYNLT1-knockout mouse model reveals electrophysiological alterations and potential mechanistic contributors to atrial fibrillation.Biology open · 2025Article
- A prognostic model for laryngeal squamous cell carcinoma based on the mitochondrial metabolism-related genes.Translational cancer research · 2025Article
- A review of the pathogenesis of mitochondria in breast cancer and progress of targeting mitochondria for breast cancer treatment.Journal of translational medicine · 2025Review
- Bioinformatics and experimental approach reveal potential prognostic and immunological roles of key mitochondrial metabolism-related genes in cervical cancer.Frontiers in oncology · 2025Article
- Mitochondria: a new intervention target for tumor invasion and metastasis.Molecular medicine (Cambridge, Mass.) · 2024Review
- Multi-Allelic Mitochondrial DNA Deletions in an Adult Dog with Chronic Weakness, Exercise Intolerance and Lactic Acidemia.Animals : an open access journal from MDPI · 2024Article
- Salidroside enhances 5-fluorouracil sensitivity against hepatocellular carcinoma via YIPF5-induced mitophagy.Frontiers in pharmacology · 2024Article
- MAST4 promotes primary ciliary resorption through phosphorylation of Tctex-1.Life science alliance · 2023Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMitochondrial metabolism has been proposed as an attractive target for breast cancer therapy. The discovery of new mechanisms underlying mitochondrial dysfunction will facilitate the development of new metabolic inhibitors to improve the clinical treatment of breast cancer patients. DYNLT1 (Dynein Light Chain Tctex-Type 1) is a key component of the motor complex that transports cellular cargo along microtubules in the cell, but whether and how DYNLT1 affects mitochondrial metabolism and breast cancer has not been reported.
methodsThe expression levels of DYNLT1 were analyzed in clinical samples and a panel of cell lines. The role of DYNLT1 in breast cancer development was investigated using in vivo mouse models and in vitro cell assays, including CCK-8, plate cloning and transwell assay. The role of DYNLT1 in regulating mitochondrial metabolism in breast cancer development is examined by measuring mitochondrial membrane potential and ATP levels. To investigate the underlying molecular mechanism, many methods, including but not limited to Co-IP and ubiquitination assay were used.
resultsFirst, we found that DYNLT1 was upregulated in breast tumors, especially in ER + and TNBC subtypes. DYNLT1 promotes the proliferation, migration, invasion and mitochondrial metabolism in breast cancer cells in vitro and breast tumor development in vivo. DYNLT1 colocalizes with voltage-dependent anion channel 1 (VDAC1) on mitochondria to regulate key metabolic and energy functions. Mechanistically, DYNLT1 stabilizes the voltage-dependent anion channel 1 (VDAC1) by hindering E3 ligase Parkin-mediated VDAC1 ubiquitination and degradation.
conclusionOur data demonstrate that DYNLT1 promotes mitochondrial metabolism to fuel breast cancer development by inhibiting Parkin-mediated ubiquitination degradation of VDAC1. This study suggests that mitochondrial metabolism can be exploited by targeting the DYNLT1-Parkin-VDAC1 axis to improve the ability of metabolic inhibitors to suppress cancers with limited treatment options, such as triple-negative breast cancer (TNBC).
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