ArticleGenes2026
Dual-Target Inhibition of CDK5 and PBK in Pituitary Neuroendocrine Tumors: Mechanisms and Therapeutic Potential.
Article in Genes, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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6 authors.
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Abstract
BACKGROUND/
objectivesPituitary neuroendocrine tumors (PitNETs) frequently exhibit invasive behaviors that complicate clinical treatment. While cyclin-dependent kinase 5 (CDK5) and lymphokine-activated killer T-cell-originated protein kinase (PBK, also known as PDZ-binding kinase) are implicated in tumor progression, their reciprocal regulatory mechanism remains unclear. This study aims to elucidate the CDK5-PBK interaction in PitNETs and identify potential therapeutic agents targeting this pathway.
methodsWe utilized proximity labeling and phospho-specific assays to characterize the CDK5 and PBK interaction in PitNET cell lines. Immunohistochemical analysis was performed on patient tumor tissues to evaluate clinical relevance. Artificial intelligence (AI)-based virtual screening was employed to discover dual-target inhibitors. The therapeutic efficacy of the identified compound, proguanil hydrochloride, was subsequently evaluated using in vitro functional assays, alongside in vivo xenograft animal models.
resultsWe identified a mutual phosphorylation loop between CDK5 (at S159) and PBK (at T9) that activates insulin signaling, thereby promoting cellular proliferation and invasion in PitNETs. Patient tumor analysis revealed that the co-expression of phosphorylated CDK5 (S159) and PBK (T9) significantly correlates with tumor invasiveness (
conclusionsThe CDK5-PBK mutual phosphorylation axis serves as a key driver of invasiveness in PitNETs. Proguanil hydrochloride represents a promising candidate dual-target therapeutic agent capable of disrupting this pathway to suppress tumor growth.
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