ArticleFrontiers in oncology2022
Functional Interaction Between the Oncogenic Kinase NEK2 and Sam68 Promotes a Splicing Program Involved in Migration and Invasion in Triple-Negative Breast Cancer.
Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Identification of circRNA/lncRNA-miRNA-Transcription Factor-mRNA Networks to Identify Potential Biomarkers in Response to Neoadjuvant Therapy for Breast Cancer.Breast cancer (Dove Medical Press) · 2026Article
- Comprehensive analysis of mitophagy-related genes reveals prognostic signatures in breast cancer: based on immune landscapes and treatment target predict.Frontiers in immunology · 2026Article
- NEK2 promotes the progression of osteosarcoma through the AKT/p-AKT pathway and interacts with FoxM1.Medical oncology (Northwood, London, England) · 2025Article
- Overexpressed NEK2 contributes to progression and cisplatin resistance through activating the Wnt/β-catenin signaling pathway in cervical cancer.Cancer cell international · 2025Article
- Role of NEK2 in tumorigenesis and tumor progression.Trends in molecular medicine · 2025Review
- Role of Sam68 in different types of cancer (Review).International journal of molecular medicine · 2025Review
- Mechanisms of RNA alternative splicing dysregulation in triple-negative breast cancer.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Review
- Differential expression of paralog RNA binding proteins establishes a dynamic splicing program required for normal cerebral cortex development.Nucleic acids research · 2024Article
- Recent Advances in Drug Discovery for Triple-Negative Breast Cancer Treatment.Molecules (Basel, Switzerland) · 2023Review
- Differential Expression of NEK Kinase Family Members in Esophageal Adenocarcinoma and Barrett's Esophagus.Cancers · 2023Article
- Article
- Validating Sam68 expression and protein level in breast cancer.Journal of medicine and life · 2023Article
- Screening of novel biomarkers for breast cancer based on WGCNA and multiple machine learning algorithms.Translational cancer research · 2023Article
- Cdk1-mediated threonine phosphorylation of Sam68 modulates its RNA binding, alternative splicing activity and cellular functions.Nucleic acids research · 2022Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) represents the most aggressive breast cancer subtype. Poor prognosis in TNBC is partly due to lack of efficacious targeted therapy and high propensity to metastasize. Dysregulation of alternative splicing has recently emerged as a trait of TNBC, suggesting that unveiling the molecular mechanisms underlying its regulation could uncover new druggable cancer vulnerabilities. The oncogenic kinase NEK2 is significantly upregulated in TNBC and contributes to shaping their unique splicing profile. Herein, we found that NEK2 interacts with the RNA binding protein Sam68 in TNBC cells and that NEK2-mediated phosphorylation of Sam68 enhances its splicing activity. Genome-wide transcriptome analyses identified the splicing targets of Sam68 in TNBC cells and revealed a common set of exons that are co-regulated by NEK2. Functional annotation of splicing-regulated genes highlighted cell migration and spreading as biological processes regulated by Sam68. Accordingly, Sam68 depletion reduces TNBC cell migration and invasion, and these effects are potentiated by the concomitant inhibition of NEK2 activity. Our findings indicate that Sam68 and NEK2 functionally cooperate in the regulation of a splicing program that sustains the pro-metastatic features of TNBC cells.
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