ArticleMolecular medicine (Cambridge, Mass.)2023
Paired protein kinases PRKCI-RIPK2 promote pancreatic cancer growth and metastasis via enhancing NF-κB/JNK/ERK phosphorylation.
Article in Molecular medicine (Cambridge, Mass.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Prognostic and clinicopathological roles of circular RNA expression in chemoresistance in head and neck squamous cell carcinoma: a systematic review.Frontiers in pharmacology · 2025Pooled it
- Targeting Prolyl 3-hydroxylase 1 inhibits pancreatic cancer progression and macrophage immunity.Nature communications · 2026Article
- RIPK2 induces docetaxel resistance in prostate cancer through the NF-κB/P-gp signaling pathway.PloS one · 2026Article
- Mechanistic insights into hepatic metastasis of pancreatic cancer: molecular perspectives.Translational gastroenterology and hepatology · 2026Review
- FUT3-B3GNT3 interaction promotes pancreatic cancer progression and chemoresistance via NF-κB signaling mediated autophagy.European journal of medical research · 2025Article
- Prkci acts a pro-proliferation factor in colorectal cancer.NPJ precision oncology · 2025Article
- Prkci promotes colorectal cancer metastasis by phosphorylating and stabilizing Tgfbr1 to activate TGF-β signaling.Cell communication and signaling : CCS · 2025Article
- Inflammation, microbiota, and pancreatic cancer.Cancer cell international · 2025Review
- Single-cell and spatial transcriptomics reveal pre-metastatic subsets and therapeutic targets in penile carcinoma.iScience · 2025Article
- Targeting the CSF1/CSF1R signaling pathway: an innovative strategy for ultrasound combined with macrophage exhaustion in pancreatic cancer therapy.Frontiers in immunology · 2024Review
- Receptor interacting serine/threonine kinase 2 promotes rheumatoid arthritis progression and partially regulates nuclear factor kappa B pathway.CytoJournal · 2024Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundProtein kinases play a pivotal role in the malignant evolution of pancreatic cancer (PC) through mediating phosphorylation. Many kinase inhibitors have been developed and translated into clinical use, while the complex pathology of PC confounds their clinical efficacy and warrants the discovery of more effective therapeutic targets.
methodsHere, we used the Gene Expression Omnibus (GEO) database and protein kinase datasets to map the PC-related protein kinase-encoding genes. Then, applying Gene Expression and Profiling Interactive Analysis (GEPIA), GEO and Human Protein Atlas, we evaluated gene correlation, gene expression at protein and mRNA levels, as well as survival significance. In addition, we performed protein kinase RIPK2 knockout and overexpression to observe effects of its expression on PC cell proliferation, migration and invasion in vitro, as well as cell apoptosis, reactive oxygen species (ROS) production and autophagy. We established PC subcutaneous xenograft and liver metastasis models to investigate the effects of RIPK2 knockout on PC growth and metastasis. Co-immunoprecipitation and immunofluorescence were utilized to explore the interaction between protein kinases RIPK2 and PRKCI. Polymerase chain reaction and immunoblotting were used to evaluate gene expression and protein phosphorylation level.
resultsWe found fourteen kinases aberrantly expressed in human PC and nine kinases with prognosis significance. Among them, RIPK2 with both serine/threonine and tyrosine activities were validated to promote PC cells proliferation, migration and invasion. RIPK2 knockout could inhibit subcutaneous tumor growth and liver metastasis of PC. In addition, RIPK2 knockout suppressed autophagosome formation, increased ROS production and PC cell apoptosis. Importantly, another oncogenic kinase PRKCI could interact with RIPK2 to enhance the phosphorylation of downstream NF-κB, JNK and ERK.
conclusionPaired protein kinases PRKCI-RIPK2 with multiple phosphorylation activities represent a new pathological mechanism in PC and could provide potential targets for PC therapy.
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