Assessment of cholecystokinin 2 receptor (CCK2R) in neoplastic tissue

Roy, Jyoti; Putt, Karson S.; Coppola, Domenico; Leon, Marino E.; Khalil, Farah; Centeno, Barbara A.; Clark, Noel; Stark, Valerie E.; Morse, David L.

doi:10.18632/oncotarget.7522

Cited by 39 publications

(40 citation statements)

References 40 publications

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“…Table 2 summarizes the localization and actions of gastrin, CCK, and their receptors on different types of human cancers (indicated as percentage of positive tissues expressing the corresponding ligand or receptor). A variety of human adenocarcinomas in the stomach, pancreas, colon, rectum, esophagus, lung, liver, medullary thyroid, overexpress CCK2R and/or CCK1R than the matched normal tissues (61,62,71,79,81,82), serving as the basis for CCK2R-or CCK1Rtargeted tumor imaging and therapy (84). Indeed, intensive chemical, physiological, and pharmacological studies provide novel diagnostic and therapeutic agents for the tumors overexpressing CCK2R and/or CCK1R (85).…”

Section: The Receptors For Gastrin and Cckmentioning

confidence: 99%

Gastrin, Cholecystokinin, Signaling, and Biological Activities in Cellular Processes

Zeng¹,

Ou²,

Wang³

et al. 2020

Front. Endocrinol.

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The structurally-related peptides, gastrin and cholecystokinin (CCK), were originally discovered as humoral stimulants of gastric acid secretion and pancreatic enzyme release, respectively. With the aid of methodological advances in biochemistry, immunochemistry, and molecular biology in the past several decades, our concept of gastrin and CCK as simple gastrointestinal hormones has changed considerably. Extensive in vitro and in vivo studies have shown that gastrin and CCK play important roles in several cellular processes including maintenance of gastric mucosa and pancreatic islet integrity, neurogenesis, and neoplastic transformation. Indeed, gastrin and CCK, as well as their receptors, are expressed in a variety of tumor cell lines, animal models, and human samples, and might contribute to certain carcinogenesis. In this review, we will briefly introduce the gastrin and CCK system and highlight the effects of gastrin and CCK in the regulation of cell proliferation and apoptosis in both normal and abnormal conditions. The potential imaging and therapeutic use of these peptides and their derivatives are also summarized.

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Section: The Receptors For Gastrin and Cckmentioning

confidence: 99%

Gastrin, Cholecystokinin, Signaling, and Biological Activities in Cellular Processes

Zeng¹,

Ou²,

Wang³

et al. 2020

Front. Endocrinol.

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“…In contrast, the expression of other receptors in normal tissues must be considered when targeting ligands are assessed for use as imaging or therapeutic agents. In addition, normal tissue samples from the primary tumor organ site should be scrutinized prior to a receptor’s designation as an overexpressed or upregulated entity, and normal tissues from multiple organ sites for concern for toxicity should be examined prior to the determination of a marker as an appropriate entity for the ligand targeting of therapeutic agents, or for concern for background signal interference prior to the targeting of imaging agents [ 265 ].…”

Section: Discussionmentioning

confidence: 99%

Exploiting cancer’s phenotypic guise against itself: targeting ectopically expressed peptide G-protein coupled receptors for lung cancer therapy

et al. 2017

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Lung cancer, claiming millions of lives annually, has the highest mortality rate worldwide. This advocates the development of novel cancer therapies that are highly toxic for cancer cells but negligibly toxic for healthy cells. One of the effective treatments is targeting overexpressed surface receptors of cancer cells with receptor-specific drugs. The receptors-in-focus in the current review are the G-protein coupled receptors (GPCRs), which are often overexpressed in various types of tumors. The peptide subfamily of GPCRs is the pivot of the current article owing to the high affinity and specificity to and of their cognate peptide ligands, and the proven efficacy of peptide-based therapeutics. The article summarizes various ectopically expressed peptide GPCRs in lung cancer, namely, Cholecystokinin-B/Gastrin receptor, the Bombesin receptor family, Bradykinin B1 and B2 receptors, Arginine vasopressin receptors 1a, 1b and 2, and the Somatostatin receptor type 2. The autocrine growth and pro-proliferative pathways they mediate, and the distinct tumor-inhibitory effects of somatostatin receptors are then discussed. The next section covers how these pathways may be influenced or ‘corrected’ through therapeutics (involving agonists and antagonists) targeting the overexpressed peptide GPCRs. The review proceeds on to Nano-scaled delivery platforms, which enclose chemotherapeutic agents and are decorated with peptide ligands on their external surface, as an effective means of targeting cancer cells. We conclude that targeting these overexpressed peptide GPCRs is potentially evolving as a highly promising form of lung cancer therapy.

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“…Gastrin binds to the cholecystokinin-2 receptor (CCK-2R), activates phosphoinositide3 kinase (PI3K)/Akt and JAK-STAT3 signaling pathways, and effect on adherence of host cells[ 45 ]. CCK-2R upregulates in different types of cancers[ 46 ]. This event cause loss of acid producing cells and deregulates expression of some growth factors that influence on cell differentiation[ 47 ].…”

Section: H Pylori Infection and Interruption Of Host Signalmentioning

confidence: 99%

New insights ofHelicobacter pylorihost-pathogen interactions: The triangle of virulence factors, epigenetic modifications and non-coding RNAs

Vaziri

Tarashi

Fateh

et al. 2018

WJCC

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Helicobacter pylori (H. pylori) is a model organism for understanding host-pathogen interactions and infection-mediated carcinogenesis. Gastric cancer and H. pylori colonization indicates the strong correlation. The progression and exacerbation of H. pylori infection are influenced by some factors of pathogen and host. Several virulence factors involved in the proper adherence and attenuation of immune defense to contribute the risk of emerging gastric cancer, therefore analysis of them is very important. H. pylori also modulates inflammatory and autophagy process to intensify its pathogenicity. From the host regard, different genetic factors particularly affect the development of gastric cancer. Indeed, epigenetic modifications, MicroRNA and long non-coding RNA received more attention. Generally, various factors related to pathogen and host that modulate gastric cancer development in response to H. pylori need more attention due to develop an efficacious therapeutic intervention. Therefore, this paper will present a brief overview of host-pathogen interaction especially emphases on bacterial virulence factors, interruption of host cellular signaling, the role of epigenetic modifications and non-coding RNAs.

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Assessment of cholecystokinin 2 receptor (CCK2R) in neoplastic tissue

Cited by 39 publications

References 40 publications

Gastrin, Cholecystokinin, Signaling, and Biological Activities in Cellular Processes

Gastrin, Cholecystokinin, Signaling, and Biological Activities in Cellular Processes

Exploiting cancer’s phenotypic guise against itself: targeting ectopically expressed peptide G-protein coupled receptors for lung cancer therapy

New insights ofHelicobacter pylorihost-pathogen interactions: The triangle of virulence factors, epigenetic modifications and non-coding RNAs

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