ArticleNature communications2022
TUBB4A interacts with MYH9 to protect the nucleus during cell migration and promotes prostate cancer via GSK3β/β-catenin signalling.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 64 citations in OpenAlex.
- SLC38A7 promotes gastric cancer progression through activating Wnt/β-catenin signaling via interaction with MYH9.Chinese medical journal · 2026Article
- A Cell Type-Specific Role for Tubb6 in Ciliogenesis of Xenopus Epidermal Multiciliated Cells.Cytoskeleton (Hoboken, N.J.) · 2026Article
- MYH9: Structure, functions, and therapeutic implications in cancer and genetic disorders.Genes & diseases · 2026Review
- Carbonyl stress by glyceraldehyde promotes glycation of nuclear non-muscle myosins in DNA-protein crosslink assemblies.Journal of clinical biochemistry and nutrition · 2026Article
- STAT1 accelerates cutaneous melanoma progression through TUBB4A expression regulation.Molecular medicine reports · 2026Article
- Targeting KIF23 inhibits cell proliferation and primary chemoresistance in cervical cancer by inactivating the MYH9/MCM2/PCNA pathway.Clinical and translational medicine · 2026Article
- Cancer-associated SF3B1 mutation suppresses DNA repair by disrupting the organization of nuclear actin network.Cell death & disease · 2026Article
- PLOD2 promotes proliferation, migration and invasion of colorectal cancer cells via PI3K-AKT-GSK3β signaling pathway.Scientific reports · 2026Article
- Volumetric mechanoplasticity couples melanoma drug tolerance to susceptibility to CD8bioRxiv : the preprint server for biology · 2026Article
- CD73 overexpression in ADSCs accelerates bladder repair by regulating the NFκB/NLRP3/caspase-1 signaling axis in neurogenic bladder rats.NPJ Regenerative medicine · 2026Article
- Third-generation whole-genome sequencing reveals the role of CNTNAP2 as a tumor suppressor gene in high-risk neuroblastomas.Journal of translational medicine · 2026Article
- Hsa_circ_0030568 Promotes the Proliferation and Migration of Prostate Cancer CellsCombinatorial chemistry & high throughput screening · 2026Article
- Lactylation-driven KRT19 promotes non-small cell lung cancer progression by suppressing cellular senescence.Journal of experimental & clinical cancer research : CR · 2025Article
- Signalling pathways in a nutshell: from pathogenesis to therapeutical implications in prostate cancer.Annals of medicine · 2025Review
- A novel lncRNA, Lnc21q22.11, suppresses gastric cancer growth by inhibiting MEK/ERK pathway.Epigenetics · 2025Article
- RCC2 and CD24 cooperate to modulate prostate cancer progression through vimentin ubiquitination and β-catenin activation.The Journal of clinical investigation · 2025Article
- PLAURAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- ARHGAP4/MYH9/β-catenin/c-Jun positive feedback loop promotes colorectal cancer stemness.NPJ precision oncology · 2025Article
- Antibody MYH9 and Antibiotic Lidamycin Inhibit the Growth and Proliferation of Lung Cancer Cells and Induce Their Apoptosis.Molecular biotechnology · 2025Article
- The class II myosin MYH4 safeguards genome integrity and suppresses tumor progression.The Journal of clinical investigation · 2025Article
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
Human tubulin beta class IVa (TUBB4A) is a member of the β-tubulin family. In most normal tissues, expression of TUBB4A is little to none, but it is highly expressed in human prostate cancer. Here we show that high expression levels of TUBB4A are associated with aggressive prostate cancers and poor patient survival, especially for African-American men. Additionally, in prostate cancer cells, TUBB4A knockout (KO) reduces cell growth and migration but induces DNA damage through increased γH2AX and 53BP1. Furthermore, during constricted cell migration, TUBB4A interacts with MYH9 to protect the nucleus, but either TUBB4A KO or MYH9 knockdown leads to severe DNA damage and reduces the NF-κB signaling response. Also, TUBB4A KO retards tumor growth and metastasis. Functional analysis reveals that TUBB4A/GSK3β binds to the N-terminal of MYH9, and that TUBB4A KO reduces MYH9-mediated GSK3β ubiquitination and degradation, leading to decreased activation of β-catenin signaling and its relevant epithelial-mesenchymal transition. Likewise, prostate-specific deletion of Tubb4a reduces spontaneous tumor growth and metastasis via inhibition of NF-κB, cyclin D1, and c-MYC signaling activation. Our results suggest an oncogenic role of TUBB4A and provide a potentially actionable therapeutic target for prostate cancers with TUBB4A overexpression.
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