ArticleCancer gene therapy2022
Targeting CLK4 inhibits the metastasis and progression of breast cancer by inactivating TGF-β pathway.
Article in Cancer gene therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Decoding SR protein regulation: kinases, phosphatases, and therapeutic targeting strategies.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Novel Pyrrolopyrimidines as Inhibitors of CLK4 and HER2: Targeting Promising Anticancer Pathways.Medicinal chemistry (Shariqah (United Arab Emirates)) · 2026Article
- Investigating the Mechanism of Astragalus mongholicus-Mediated Treatment of Silicosis in Mice from the Perspective of Alternative Splicing.Current drug targets · 2026Article
- Computational screening and molecular dynamics of natural compounds targeting the SH2 domain of STAT3: a multitarget approach using network pharmacology.Molecular diversity · 2025Article
- Pharmacological CLK inhibition disrupts SR protein function and RNA splicing blocking cell growth and migration in TNBC.Breast cancer research : BCR · 2025Article
- Identification and Biological Evaluation of a Novel CLK4 Inhibitor Targeting Alternative Splicing in Pancreatic Cancer Using Structure-Based Virtual Screening.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- An update on cancer stem cell survival pathways involved in chemoresistance in triple-negative breast cancer.Future oncology (London, England) · 2025Review
- Targeting RNA splicing modulation: new perspectives for anticancer strategy?Journal of experimental & clinical cancer research : CR · 2025Review
- Development of 5-hydroxybenzothiophene derivatives as multi-kinase inhibitors with potential anti-cancer activity.Future medicinal chemistry · 2024Article
- SLC12A8 mediates TKI resistance in EGFR-mutant lung cancer via PDK1/AKT axis.Journal of cancer research and clinical oncology · 2023Article
- Cdc2-like kinases: structure, biological function, and therapeutic targets for diseases.Signal transduction and targeted therapy · 2023Review
- Targeting cancer stem cell plasticity in triple-negative breast cancer.Exploration of targeted anti-tumor therapy · 2023Review
- High-Altitude Stress Orchestrates mRNA Expression and Alternative Splicing of Ovarian Follicle Development Genes in Tibetan Sheep.Animals : an open access journal from MDPI · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 3 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) represents the most aggressive subtype of breast cancer that is highly resistant to current therapeutic options. According to the public databases Oncomine and KM plotter, the CLK4 expression is correlated with poor patient survival in TNBC, especially in mesenchymal-like TNBC (MES-TNBC) that has strong metastatic potential. Therefore, we investigated the potential involvement of CLK4 in the metastasis and progression of MES-TNBC. In the MES-TNBC cell lines, the CLK4 expression was elevated. Notably, the RNAi-mediated silencing of CLK4 reduced the expression of multiple epithelial-mesenchymal transition (EMT) genes that mediate metastasis. Furthermore, CLK4 silencing reduced both the invasive behaviors of the cultured cells and tumor metastasis in the mouse xenograft model. It is also noteworthy that CLK4 silencing repressed the invasive and cancer stem cell (CSC) properties that are induced by the TGF-β signaling. Importantly, the pharmacological inhibition of CLK4 potently repressed the invasion and proliferation of MES-TNBC cell lines and patient-derived cells, which demonstrates its clinical applicability. Collectively, our results suggest that CLK4 plays a crucial role in invasion and proliferation of MES-TNBC, especially in the processes that are induced by TGF-β. Also, this study characterizes CLK4 as a novel therapeutic target in breast cancer.
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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.