Adhesion Molecules as Potential Novel Biomarkers for Opioid Dependence

Liu, Yu Li; Kuo, Hsin‐Wei; Fang, Chiu‐Ping; Tsung, Jieh-Hen; Chen, Andrew C. H.

doi:10.2174/1381612826666200116144147

Cited by 4 publications

(4 citation statements)

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“…Following a lethal dose of heroin, levels of NCAMs are increased in the hippocampus of postmortem brains from people with heroin addiction, which positively correlate with blood levels of heroin at the time of death ( Weber et al, 2006 ). Levels of CDH-2 in peripheral plasma have been shown to be a potential biomarker for methadone treatment outcome, correlating with treatment success ( Liu et al, 2020 ), while hippocampal RNA expression of CDH-2 is increased following oxycodone self-administration ( Zhang et al, 2015 ). However, this effect is specific to adult, but not adolescent mice, suggesting developmental stage may moderate the role of CAMs in opioid self-administration.…”

Section: Role For Extracellular Matrix Signaling Proteins In Opioid U...mentioning

confidence: 99%

A Glitch in the Matrix: The Role of Extracellular Matrix Remodeling in Opioid Use Disorder

Ray

Williams

Kuppe

et al. 2022

Front. Integr. Neurosci.

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Opioid use disorder (OUD) and deaths from drug overdoses have reached unprecedented levels. Given the enormous impact of the opioid crisis on public health, a more thorough, in-depth understanding of the consequences of opioids on the brain is required to develop novel interventions and pharmacological therapeutics. In the brain, the effects of opioids are far reaching, from genes to cells, synapses, circuits, and ultimately behavior. Accumulating evidence implicates a primary role for the extracellular matrix (ECM) in opioid-induced plasticity of synapses and circuits, and the development of dependence and addiction to opioids. As a network of proteins and polysaccharides, including cell adhesion molecules, proteases, and perineuronal nets, the ECM is intimately involved in both the formation and structural support of synapses. In the human brain, recent findings support an association between altered ECM signaling and OUD, particularly within the cortical and striatal circuits involved in cognition, reward, and craving. Furthermore, the ECM signaling proteins, including matrix metalloproteinases and proteoglycans, are directly involved in opioid seeking, craving, and relapse behaviors in rodent opioid models. Both the impact of opioids on the ECM and the role of ECM signaling proteins in opioid use disorder, may, in part, depend on biological sex. Here, we highlight the current evidence supporting sex-specific roles for ECM signaling proteins in the brain and their associations with OUD. We emphasize knowledge gaps and future directions to further investigate the potential of the ECM as a therapeutic target for the treatment of OUD.

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Section: Role For Extracellular Matrix Signaling Proteins In Opioid U...mentioning

confidence: 99%

A Glitch in the Matrix: The Role of Extracellular Matrix Remodeling in Opioid Use Disorder

Ray

Williams

Kuppe

et al. 2022

Front. Integr. Neurosci.

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“…Several of their regulators have been experimentally validated as drivers of oncogenesis, tumor progression, and metastasis in ccRCC, suggesting possible transcriptional mechanisms through which opioids may affect ccRCC development and metastasis. Notably, CDH2, the MR with the strongest enrichment score, is known to be involved in the opioid pathway, and CDH2 variants influence methadone response (37,38). MRs associated with other survival-related networks were also tightly linked with opioid pathway (Fig.…”

Section: Reconstructing Directed Transcriptional Network and Mrs Of R...mentioning

confidence: 95%

Identifying Clear Cell Renal Cell Carcinoma Coexpression Networks Associated with Opioid Signaling and Survival

et al. 2021

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While opioids constitute the major component of perioperative analgesic regimens for surgery in general, a variety of evidence points to an association between perioperative opioid exposure and longer term oncologic outcomes. The mechanistic details underlying these effects are not well understood. In this study, we focused on clear cell renal cell carcinoma (ccRCC) and utilized RNA sequencing and outcome data from both The Cancer Genome Atlas, as well as a local patient cohort to identify survival-associated gene coexpression networks. We then projected drug-induced transcriptional profiles from in vitro cancer cells to predict drug effects on these networks and recurrence-free, cancer-specific, and overall survival. The opioid receptor agonist, leu-enkephalin, was predicted to have antisurvival effects in ccRCC, primarily through Th2 immune- and NRF2-dependent macrophage networks. Conversely, the antagonist, naloxone, was predicted to have prosurvival effects, primarily through angiogenesis, fatty acid metabolism, and hemopoesis pathways. Eight coexpression networks associated with survival endpoints in ccRCC were identified, and master regulators of the transition from the normal to disease state were inferred, a number of which are linked to opioid pathways. These results are the first to suggest a mechanism for opioid effects on cancer outcomes through modulation of survival-associated coexpression networks. While we focus on ccRCC, this methodology may be employed to predict opioid effects on other cancer types and to personalize analgesic regimens in patients with cancer for optimal outcomes. Significance: This study suggests a possible molecular mechanism for opioid effects on cancer outcomes generally, with implications for personalization of analgesic regimens.

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“…As well as these potential applications in cancer diagnosis, increased levels of soluble Nectin-4 in serum may contribute to the diagnosis and monitoring of asthma ( 62 ) and may also represent a new biomarker for opioid dependence ( 63 , 64 ). To date, most research has focused on Nectin-4 as a transmembrane protein of tumor cells, with less attention paid to soluble Nectin-4.…”

Section: Diagnostic Potential Of Nectin-4mentioning

confidence: 99%

Therapeutic prospects of nectin-4 in cancer: applications and value

Li,

Zhou,

Zang

et al. 2024

Front. Oncol.

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Nectin-4 is a Ca2+-independent immunoglobulin-like protein that exhibits significantly elevated expression in malignant tumors while maintaining extremely low levels in healthy adult tissues. In recent years, overexpression of Nectin-4 has been implicated in tumor occurrence and development of various cancers, including breast cancer, urothelial cancer, and lung cancer. In 2019, the Food and Drug Administration approved enfortumab vedotin, the first antibody–drug conjugate targeting Nectin-4, for the treatment of urothelial carcinoma. This has emphasized the value of Nectin-4 in tumor targeted therapy and promoted the implementation of more clinical trials of enfortumab vedotin. In addition, many new drugs targeting Nectin-4 for the treatment of malignant tumors have entered clinical trials, with the aim of exploring potential new indications. However, the exact mechanisms by which Nectin-4 affects tumorigenesis and progression are still unclear, and the emergence of drug resistance and treatment-related adverse reactions poses challenges. This article reviews the diagnostic potential, prognostic significance, and molecular role of Nectin-4 in tumors, with a focus on clinical trials in the field of Nectin-4-related tumor treatment and the development of new drugs targeting Nectin-4.

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Adhesion Molecules as Potential Novel Biomarkers for Opioid Dependence

Cited by 4 publications

References 0 publications

A Glitch in the Matrix: The Role of Extracellular Matrix Remodeling in Opioid Use Disorder

A Glitch in the Matrix: The Role of Extracellular Matrix Remodeling in Opioid Use Disorder

Identifying Clear Cell Renal Cell Carcinoma Coexpression Networks Associated with Opioid Signaling and Survival

Therapeutic prospects of nectin-4 in cancer: applications and value

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