ArticleJournal of experimental & clinical cancer research : CR2021
Actin-like protein 6A/MYC/CDK2 axis confers high proliferative activity in triple-negative breast cancer.
Article in Journal of experimental & clinical cancer research : CR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Overexpression of ACTL6A is associated with poor prognosis in gastric cancer, and nuclear level is an independent predictor.Translational cancer research · 2026Article
- Predicting bevacizumab efficacy: the emerging role of ACTL6B in colorectal cancer.Journal of gastrointestinal oncology · 2025Article
- Inhibition of tumor-intrinsic NAT10 enhances antitumor immunity by triggering type I interferon response via MYC/CDK2/DNMT1 pathway.Nature communications · 2025Article
- CDK2 inhibition sensitizes anthracycline-induced immunogenic cell death and enhances the efficacy of anti-PD-1 therapy.Frontiers in immunology · 2025Article
- Actin-Like Protein 6A as an Oncogene and Therapeutic Target in Cancer.International journal of medical sciences · 2025Review
- Circ_0084615 promotes epithelial-mesenchymal transition-mediated tumor progression in hepatocellular carcinoma.Annals of gastroenterological surgery · 2024Article
- Extracellular vesicle-mediated delivery of miR-766-3p from bone marrow stromal cells as a therapeutic strategy against colorectal cancer.Cancer cell international · 2024Article
- Transcriptional pausing induced by ionizing radiation enables the acquisition of radioresistance in nasopharyngeal carcinoma.Journal of molecular cell biology · 2024Article
- Fur removal promotes an earlier expression of involution-related genes in mammary gland of lactating mice.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2023Article
- Small-molecule exhibits anti-tumor activity by targeting the RNA mAmerican journal of cancer research · 2023Article
- Risk stratification based on DNA damage-repair-related signature reflects the microenvironmental feature, metabolic status and therapeutic response of breast cancer.Frontiers in immunology · 2023Article
- A review on the role of cyclin dependent kinases in cancers.Cancer cell international · 2022Review
- Abrine Elicits Liver Carcinoma Immunity and Enhances Antitumor Efficacy of Immune Checkpoint Blockade by Modulating PD-L1 Signaling.Journal of oncology · 2022Article
- Article
- Potential Role of SWI/SNF Complex Subunit Actin-Like Protein 6A in Cervical Cancer.Frontiers in oncology · 2021Article
- Upregulated Expression of Actin-Like 6A is a Risk Factor Affecting the Prognosis of Pancreatic Cancer.Cancer management and research · 2021Article
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundTriple negative breast cancer (TNBC) is an aggressive subtype of breast cancer with high proliferative activity. TNBC tumors exhibit elevated MYC expression and altered expression of MYC regulatory genes, which are associated with tumor progression and poor prognosis; however, the underlying mechanisms by which MYC retains its high expression and mediates TNBC tumorigenesis require further exploration.
methodsACTL6A regulation of MYC and its target gene, CDK2, was defined using Co-IP, mass spectrometry and ChIP assays. To study the role of ACTL6A in TNBC, we performed soft-agar, colony formation, flow cytometry and tumor formation in nude mice. CDK2 inhibitor and paclitaxel were used in testing combination therapy in vitro and in vivo.
resultsACTL6A bound MYC to suppress glycogen synthase kinase 3 beta (GSK3β)-induced phosphorylation on MYC T58, which inhibited ubiquitination of MYC and stabilized it. Moreover, ACTL6A promoted the recruitment of MYC and histone acetyltransferase KAT5 on CDK2 promoters, leading to hyperactivation of CDK2 transcription. ACTL6A overexpression promoted, while silencing ACTL6A suppressed cell proliferation and tumor growth in TNBC cells in vitro and in vivo, which was dependent on MYC signaling. Furthermore, co-therapy with paclitaxel and CDK2 inhibitor showed synergistic effects in tumor suppression. Notably, ACTL6A/MYC/CDK2 axis was specifically up-regulated in TNBC and high expression of ACTL6A was correlated to shorter survival in patients with TNBC.
conclusionsThese findings reveal a novel mechanism by which ACTL6A prolongs the retention of MYC in TNBC and suggest that pharmacological targeting ACTL6A/MYC/CDK2 axis might have therapeutic potential in patients with TNBC.
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