ArticleOncogene2017
Upregulation of MARCKS in kidney cancer and its potential as a therapeutic target.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed.
- Integrated multi-omics analysis reveals that MARCKS reprograms the immunosuppressive microenvironment to drive hepatocellular carcinoma progression.NPJ precision oncology · 2026Article
- Venous endothelial remodeling mediated byFrontiers in immunology · 2026Article
- Cancer biomarkers discovered using pan-cancer plasma proteomic profiling.Nature biomedical engineering · 2026Article
- Article
- Nuclear transport of phosphorylated LanCL2 promotes invadopodia formation and tumor progression of glioblastoma by activating STAT3/Cortactin signaling.Journal of advanced research · 2025Article
- LINC01133 regulates MARCKS expression via sponging miR-30d-5p to promote the development of lung squamous cell carcinoma.Translational oncology · 2024Article
- Investigating cellular similarities and differences between upper tract urothelial carcinoma and bladder urothelial carcinoma using single-cell sequencing.Frontiers in immunology · 2024Article
- Integrated single-cell RNA sequencing analysis reveals a mesenchymal stem cell-associated signature for estimating prognosis and drug sensitivity in gastric cancer.Journal of cancer research and clinical oncology · 2023Article
- Integrated analysis identifies microRNA-188-5p as a suppressor of AKT/mTOR pathway in renal cancer.Cancer science · 2023Article
- Antler-derived microRNA PC-5p-1090 inhibits HCC cell proliferation, migration, and invasion by targeting MARCKS, SMARCAD1, and SOX9.Functional & integrative genomics · 2023Article
- Article
- Review
- Hypoxia Promotes Angiogenic Effect in Extracranial Arteriovenous Malformation Endothelial Cells.International journal of molecular sciences · 2022Article
- Transcriptome Analysis of Liver Cancer Cell Huh-7 Treated With Metformin.Frontiers in pharmacology · 2022Article
- A Novel Renoprotective Strategy: Upregulation of PD-L1 Mitigates Cisplatin-Induced Acute Kidney Injury.International journal of molecular sciences · 2021Article
- The myristoylated alanine-rich C-kinase substrates (MARCKS): A membrane-anchored mediator of the cell function.Autoimmunity reviews · 2021Review
- Longitudinal single-cell profiling reveals molecular heterogeneity and tumor-immune evolution in refractory mantle cell lymphoma.Nature communications · 2021Article
- Pathophysiological roles of myristoylated alanine-rich C-kinase substrate (MARCKS) in hematological malignancies.Biomarker research · 2021Review
- SILAC-Based Quantitative Proteomic Analysis of Oxaliplatin-Resistant Pancreatic Cancer Cells.Cancers · 2021Article
- MARCKS cooperates with NKAP to activate NF-kB signaling in smoke-related lung cancer.Theranostics · 2021Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Targeted therapeutics, such as those abrogating hypoxia inducible factor (HIF)/vascular endothelial growth factor signaling, are initially effective against kidney cancer (or renal cell carcinoma, RCC); however, drug resistance frequently occurs via subsequent activation of alternative pathways. Through genome-scale integrated analysis of the HIF-α network, we identified the major protein kinase C substrate MARCKS (myristoylated alanine-rich C kinase substrate) as a potential target molecule for kidney cancer. In a screen of nephrectomy samples from 56 patients with RCC, we found that MARCKS expression and its phosphorylation are increased and positively correlate with tumor grade. Genetic and pharmacologic suppression of MARCKS in high-grade RCC cell lines in vitro led to a decrease in cell proliferation and migration. We further demonstrated that higher MARCKS expression promotes growth and angiogenesis in vivo in an RCC xenograft tumor. MARCKS acted upstream of the AKT/mTOR pathway, activating HIF-target genes, notably vascular endothelial growth factor-A. Following knockdown of MARCKS in RCC cells, the IC50 of the multikinase inhibitor regorafenib was reduced. Surprisingly, attenuation of MARCKS using the MPS (MARCKS phosphorylation site domain) peptide synergistically interacted with regorafenib treatment and decreased survival of kidney cancer cells through inactivation of AKT and mTOR. Our data suggest a major contribution of MARCKS to kidney cancer growth and provide an alternative therapeutic strategy of improving the efficacy of multikinase inhibitors.
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Registered trials
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