ArticleCell death & disease2013
A myosin-Va tail fragment sequesters dynein light chains leading to apoptosis in melanoma cells.
Article in Cell death & disease, 2013. 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, 28 citations in OpenAlex.
- circFNDC3B promotes esophageal squamous cell carcinoma progression by targeting MYO5A via miR-370-3p/miR-136-5p.BMC cancer · 2023Article
- Weighted gene co-expression network indicates that the DYNLL2 is an important regulator of chicken breast muscle development and is regulated by miR-148a-3p.BMC genomics · 2022Article
- Exploration of binary protein-protein interactions between tick-borne flaviviruses and Ixodes ricinus.Parasites & vectors · 2021Article
- Cytoskeletal Remodeling in Cancer.Biology · 2020Review
- Association between aberrant dynein cytoplasmic 1 light intermediate chain 1 expression levels, mucins and chemosensitivity in colorectal cancer.Molecular medicine reports · 2020Article
- MYO5B mutations in pheochromocytoma/paraganglioma promote cancer progression.PLoS genetics · 2020Article
- Creation of a myosin Va-TAP-tagged mouse and identification of potential myosin Va-interacting proteins in the cerebellum.Cytoskeleton (Hoboken, N.J.) · 2018Article
- MYO5A inhibition by miR-145 acts as a predictive marker of occult neck lymph node metastasis in human laryngeal squamous cell carcinoma.OncoTargets and therapy · 2018Article
- Impairing the function of MLCK, myosin Va or myosin Vb disrupts Rhinovirus B14 replication.Scientific reports · 2017Article
- Two pathways regulate cortical granule translocation to prevent polyspermy in mouse oocytes.Nature communications · 2016Article
- Non-muscle myosins in tumor progression, cancer cell invasion, and metastasis.Cytoskeleton (Hoboken, N.J.) · 2014Review
- Myosin-Va contributes to manifestation of malignant-related properties in melanoma cells.The Journal of investigative dermatology · 2013Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies proposed that myosin-Va regulates apoptosis by sequestering pro-apoptotic Bmf to the actin cytoskeleton through dynein light chain-2 (DLC2). Adhesion loss or other cytoskeletal perturbations would unleash Bmf, allowing it to bind and inhibit pro-survival Bcl2 proteins. Here, we demonstrated that overexpression of a myosin-Va medial tail fragment (MVaf) harboring the binding site for DLC2 dramatically decreased melanoma cell viability. Morphological and molecular changes, including surface blebbing, mitochondrial outer membrane permeabilization, cytochrome-c and Smac release, as well as caspase-9/-3 activation and DNA fragmentation indicated that melanoma cells died of apoptosis. Immobilized MVaf interacted directly with DLCs, but complexed MVaf/DLCs did not interact with Bmf. Overexpression of DLC2 attenuated MVaf-induced apoptosis. Thus, we suggest that, MVaf induces apoptosis by sequestering DLC2 and DLC1, thereby unleashing the pair of sensitizer and activator BH3-only proteins Bmf and Bim. Murine embryonic fibroblasts (MEFs) lacking Bim and Bmf or Bax and Bak were less sensitive to apoptosis caused by MVaf expression than wild-type MEFs, strengthening the putative role of the intrinsic apoptotic pathway in this response. Finally, MVaf expression attenuated B16-F10 solid tumor growth in mice, suggesting that this peptide may be useful as an apoptosis-inducing tool for basic and translational studies.
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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.