Mechanism and Effect of Beta-Blockers on Pancreatic Adenocarcinoma: A Literature Review

Upadhyaya, Vandan; Douedi, Steven; Garcia, Brandon; Gonzalez, Jimmy; Udongwo, Ndausung; Wei, Juanqin; Nai, Qiang; Asif, Arif; Sen, Shuvendu

doi:10.14740/jocmr4387

Cited by 4 publications

(2 citation statements)

References 35 publications

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“…Longitudinal treatment of PDAC and pancreatic epithelial cell lines with nicotine results in sensitization of the α3, α4, α5, and α7nAChR-beta-adrenergic signaling connection, and increased cell migration [120]. Others have described the noteworthy interplay between beta-adrenergic signaling and PDAC progression [127].…”

Section: Pancreatic Cancermentioning

confidence: 99%

Cholinergic Mechanisms in Gastrointestinal Neoplasia

Sampaio Moura,

Schledwitz,

Alizadeh

et al. 2024

IJMS

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Acetylcholine-activated receptors are divided broadly into two major structurally distinct classes: ligand-gated ion channel nicotinic and G-protein-coupled muscarinic receptors. Each class encompasses several structurally related receptor subtypes with distinct patterns of tissue expression and post-receptor signal transduction mechanisms. The activation of both nicotinic and muscarinic cholinergic receptors has been associated with the induction and progression of gastrointestinal neoplasia. Herein, after briefly reviewing the classification of acetylcholine-activated receptors and the role that nicotinic and muscarinic cholinergic signaling plays in normal digestive function, we consider the mechanics of acetylcholine synthesis and release by neuronal and non-neuronal cells in the gastrointestinal microenvironment, and current methodology and challenges in measuring serum and tissue acetylcholine levels accurately. Then, we critically evaluate the evidence that constitutive and ligand-induced activation of acetylcholine-activated receptors plays a role in promoting gastrointestinal neoplasia. We focus primarily on adenocarcinomas of the stomach, pancreas, and colon, because these cancers are particularly common worldwide and, when diagnosed at an advanced stage, are associated with very high rates of morbidity and mortality. Throughout this comprehensive review, we concentrate on identifying novel ways to leverage these observations for prognostic and therapeutic purposes.

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Section: Pancreatic Cancermentioning

confidence: 99%

Cholinergic Mechanisms in Gastrointestinal Neoplasia

Sampaio Moura,

Schledwitz,

Alizadeh

et al. 2024

IJMS

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“…Beta adrenoreceptors are G-protein coupled receptors that are expressed by pancreatic cancer cells ( Weddle et al, 2001 ) and have been demonstrated to prolong overall survival ( Udumyan et al, 2017 ; Renz et al, 2018 ). They play an important role in tumour growth, proliferation, and inhibition of apoptosis via protein kinase A (PKA) pathways ( Upadhyaya et al, 2020 ). The effects of beta-blockers on cancer prognosis were reported to be associated with improved overall survival among pancreatic cancer patients ( Na et al, 2018 ).…”

Section: Repurposing Drugs In Pdac Treatmentmentioning

confidence: 99%

Exploiting the molecular subtypes and genetic landscape in pancreatic cancer: the quest to find effective drugs

Elebo,

Abdel-Shafy,

Cacciatore

et al. 2023

Front. Genet.

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Pancreatic Ductal Adenocarcinoma (PDAC) is a very lethal disease that typically presents at an advanced stage and is non-compliant with most treatments. Recent technologies have helped delineate associated molecular subtypes and genetic variations yielding important insights into the pathophysiology of this disease and having implications for the identification of new therapeutic targets. Drug repurposing has been evaluated as a new paradigm in oncology to accelerate the application of approved or failed target-specific molecules for the treatment of cancer patients. This review focuses on the impact of molecular subtypes on key genomic alterations in PDAC, and the progress made thus far. Importantly, these alterations are discussed in light of the potential role of drug repurposing in PDAC.

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