ArticleOncogene2016
Mitochondrial ATAD3A combines with GRP78 to regulate the WASF3 metastasis-promoting protein.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 114 citations in OpenAlex.
- ATAD3 megadalton complex in Plasmodium falciparum is essential for mitochondrial and cellular viability.PLoS pathogens · 2026Article
- Organelle contact sites in cancer cells.Cell death & disease · 2026Review
- Mitochondrial interplay with membrane organelles in health and disease.Cell communication and signaling : CCS · 2026Review
- The role of mitochondria-associated membranes in tumorigenesis.Discover oncology · 2026Review
- Single-cell transcriptomic analysis and machine learning identify ATAD3A as a key gene that stabilizes mitochondrial-endoplasmic reticulum membranes, promoting bladder cancer progression.Journal of translational medicine · 2026Article
- Mitochondria-ER crosstalk via MAMS: Bridging cellular homeostasis and cancer progression.Apoptosis : an international journal on programmed cell death · 2026Review
- Computational characterization of GRP78 binding sites on mitochondrial GPX4: implications for targeting ferroptosis in triple-negative breast cancer.Scientific reports · 2026Article
- Extracellular vesicle-delivered siRNA targeting RCN1 suppresses acute myeloid leukemia through TFAM-dependent mtDNA-cGAS-STING signaling.Extracellular vesicles and circulating nucleic acids · 2026Article
- The role of mitochondria-endoplasmic reticulum crosstalk in colorectal cancer.Genes & diseases · 2026Review
- Mitochondrial Dysfunction in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.Physiology (Bethesda, Md.) · 2025Review
- Blocking the TCA Cycle in Cancer Cells Potentiates CD36+ T-cell-Mediated Antitumor Immunity by Suppressing ER Stress-Associated THBS2 Signaling.Cancer research · 2025Article
- The correlation between mitochondria-associated endoplasmic reticulum membranes (MAMs) and CaActa pharmacologica Sinica · 2025Review
- AMPK targets PDZD8 to trigger carbon source shift from glucose to glutamine.Cell research · 2024Article
- Knockdown of hCINAP sensitizes colorectal cancer cells to ionizing radiation.Cell cycle (Georgetown, Tex.) · 2024Article
- Article
- The value of ATAD3A as a potential biomarker for bladder cancer.Cancer medicine · 2023Article
- Identification of small molecules that suppress cell invasion and metastasis promoted by WASF3 activation.Heliyon · 2023Article
- WASF3 disrupts mitochondrial respiration and may mediate exercise intolerance in myalgic encephalomyelitis/chronic fatigue syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- ATAD3A: A Key Regulator of Mitochondria-Associated Diseases.International journal of molecular sciences · 2023Review
- Role of Mitochondria-ER Contact Sites in Mitophagy.Biomolecules · 2023Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
AAA domain containing 3A (ATAD3A) is an integral mitochondrial membrane protein with unknown function, although we now show that high-level expression is associated with poor survival in breast cancer patients. Using a mass spectrometry approach we have demonstrated that ATAD3A interacts with the WASF3 metastasis-promoting protein. Knockdown of ATAD3A leads to decreased WASF3 protein levels in breast and colon cancer cells. Silencing ATAD3A also results in loss of both cell anchorage-independent growth and invasion and suppression of tumor growth and metastasis in vivo using immuno-compromised mice. HSP70 is responsible for stabilizing WASF3 in the cytoplasm, but inactivation of HSP70 does not lead to the loss of WASF3 stability at the mitochondrial membrane, where presumably it is protected through its interaction with ATAD3A. In response to endoplasmic reticulum (ER) stress, increases in the GRP78 protein level leads to increased WASF3 protein levels. We also show that ATAD3A was present in a WASF3-GRP78 complex, and suppression of GRP78 led to destabilization of WASF3 at the mitochondrial membrane, which was ATAD3A dependent. Furthermore, ATAD3A-mediated suppression of CDH1/E-cadherin occurs through its regulation of GRP78-mediated WASF3 stability. Proteolysis experiments using isolated mitochondria demonstrates the presence of the N-terminal end of WASF3 within the mitochondria, which is the interaction site with the N-terminal end of ATAD3A. It appears, therefore, that stabilization of WASF3 function occurs through its interaction with ATAD3A and GRP78, which may provide a bridge between the ER and mitochondria, allowing communication between the two organelles. These findings also suggest that pharmacologic inhibition of ATAD3A could be an effective therapeutic strategy to treat human cancer.
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Registered trials
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.