ArticleCell death & disease2018
Actin like-6A promotes glioma progression through stabilization of transcriptional regulators YAP/TAZ.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
45 citing papers in PubMed, 79 citations in OpenAlex.
- Actin, connexin-43 and GAP-43 expression in gliomas: real-world associations with IDH status, tumor burden and survival.Journal of neuro-oncology · 2026Article
- YAP/TEAD complex restricts H3K27ac deposition to suppress testosterone synthesis in adult Leydig cells.Histochemistry and cell biology · 2026Article
- Piezo1 in the central nervous system: decoding the mechanical signature of neuroinflammation.Journal of neuroinflammation · 2026Review
- Overexpression of ACTL6A is associated with poor prognosis in gastric cancer, and nuclear level is an independent predictor.Translational cancer research · 2026Article
- HSPA5 promotes YAP/TAZ stability independently of the Hippo pathway and induces proneural-to-mesenchymal transition in glioblastoma.Cell death & disease · 2026Article
- Mechanosensitive Ion Channels: Molecular Hubs Integrating Skeletal Muscle Adaptation and Systemic Homeostasis.International journal of biological sciences · 2026Review
- ACTL6A depletion induces KLF4-mediated anti-tumorigenic effects in colorectal cancer.Cell death & disease · 2025Article
- Xenotropic and polytropic retrovirus receptor 1 (XPR1) promotes progression of papillary thyroid carcinoma via the BRAF-ERK1/2-P53 signaling pathway.Journal of endocrinological investigation · 2025Article
- YAP/TAZ-associated cell signaling - at the crossroads of cancer and neurodevelopmental disorders.Frontiers in cell and developmental biology · 2025Review
- Article
- Actin-Like Protein 6A as an Oncogene and Therapeutic Target in Cancer.International journal of medical sciences · 2025Review
- The epigenetic mechanisms involved in the treatment resistance of glioblastoma.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- Actin like 6A is a prognostic biomarker and associated with immune cell infiltration in cancers.Discover oncology · 2024Article
- YAP, TAZ, and Hippo-Dysregulating Fusion Proteins in Cancer.Annual review of cancer biology · 2024Article
- Gene amplification of chromatin remodeling factorOncology letters · 2024Article
- ACTL6A: unraveling its prognostic impact and paving the way for targeted therapeutics in carcinogenesis.Frontiers in molecular biosciences · 2024Article
- Review
- YAP/TAZ: Molecular pathway and disease therapy.MedComm · 2023Review
- ACTL6A protects gastric cancer cells against ferroptosis through induction of glutathione synthesis.Nature communications · 2023Article
- A Comprehensive Analysis Revealing FBXW9 as a Potential Prognostic and Immunological Biomarker in Breast Cancer.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increased Actin-like 6A (ACTL6A) expression has been implicated in the development of diverse cancers and recently associated with the Hippo signaling pathway, which is known to regulate biological properties, including proliferation, tissue regeneration, stem cell biology, as well as tumorigenesis. Here we first show that ACTL6A is upregulated in human gliomas and its expression is associated with glioma patient survival. ACTL6A promotes malignant behaviors of glioma cells in vitro and in orthotopic xenograft model. In co-immunoprecipitation assays, we discover that ACTL6A physically associated with YAP/TAZ and furthermore disrupts the interaction between YAP and β-TrCP E3 ubiquitin ligase, which promotes YAP protein degradation. Moreover, effects of ACTL6A on glioma cells proliferation, migration, and invasion could be mediated by YAP/TAZ. These data indicate that ACTL6A may contribute to cancer progression by stabilizing YAP/TAZ and therefore provide a novel therapeutic target for the treatment of human gliomas.
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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.