Neuroplastinβ-mediated upregulation of solute carrier family 22 member 18 antisense (SLC22A18AS) plays a crucial role in the epithelial-mesenchymal transition, leading to lung cancer cells' enhanced motility

Bajkowska, Karolina; Sumardika, I Wayan; Tomonobu, Nahoko; Chen, Youyi; Yamamoto, Ken; Kinoshita, Rie; Murata, Hitoshi; Komalasari, Ni Luh Gede Yoni; Jiang, Fan; Yamauchi, Akira; Ruma, I Made Winarsa; Kasano-Camones, Carlos Ichiro; Inoue, Yusuke; Sakaguchi, Masakiyo

doi:10.1016/j.bbrep.2020.100768

Cited by 4 publications

(3 citation statements)

References 36 publications

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“…The same inquiry would apply for the SLC22A18AS gene, in which further studies are needed to unravel its role in lung tumorigenesis and the prognosis of the disease. Although a little headway has been recently made, Bajkowska et al attributed to SLC22A18AS a key role in the epithelial-mesenchymal transition through the NPTNβ pathway in lung cancer cells, with higher cellular motility and invasion but not growth [48].…”

Section: Discussionmentioning

confidence: 99%

The Roles of Imprinted SLC22A18 and SLC22A18AS Gene Overexpression Caused by Promoter CpG Island Hypomethylation as Diagnostic and Prognostic Biomarkers for Non-Small Cell Lung Cancer Patients

Noguera-Uclés

Boyero

Salinas

et al. 2020

Cancers

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Genomic imprinting is a process that involves one gene copy turned-off in a parent-of-origin-dependent manner. The regulation of imprinted genes is broadly dependent on promoter methylation marks, which are frequently associated with both oncogenes and tumor suppressors. The purpose of this study was to assess the DNA methylation patterns of the imprinted solute-carrier family 22 member 18 (SLC22A18) and SLC22A18 antisense (SLC22A18AS) genes in non-small cell lung cancer (NSCLC) patients to study their relevance to the disease. We found that both genes were hypomethylated in adenocarcinoma and squamous cell carcinoma patients. Due to this imprinting loss, SLC22A18 and SLC22A18AS were found to be overexpressed in NSCLC tissues, which is significantly more evident in lung adenocarcinoma patients. These results were validated through analyses of public databases of NSCLC patients. The reversed gene profile of both genes was achieved in vitro by treatment with ademetionine. We then showed that high SLC22A18 and SLC22A18AS expression levels were significantly associated with worsening disease progression. In addition, low levels of SLC22A18AS were also correlated with better overall survival for lung adenocarcinoma patients. We found that SLC22A18 and SLC22A18AS knockdown inhibits cell proliferation in vitro. All these results suggest that both genes may be useful as diagnostic and prognostic biomarkers in NSCLC, revealing novel therapeutic opportunities.

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Section: Discussionmentioning

confidence: 99%

The Roles of Imprinted SLC22A18 and SLC22A18AS Gene Overexpression Caused by Promoter CpG Island Hypomethylation as Diagnostic and Prognostic Biomarkers for Non-Small Cell Lung Cancer Patients

Noguera-Uclés

Boyero

Salinas

et al. 2020

Cancers

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“…In lung cancer cells, S100A8/A9 can bind to overexpressed NPTNβ, activating transcription factors NFIA by TRAF2 and RAS signaling, and ultimately promotes cellular spheroidal growth, migration, and invasion through downstream molecules SAM pointed-domain containing E26 transformation-specific transcription factor (SPDEF) ( Sumardika et al, 2019 ). SPDEF plays a vital role in NPTNβ functions and the NPTNβ–SPDEF-induced solute carrier family 22 member 18 antisense (SLC22A18AS) is essential for EMT and cellular motility in lung cancer, with a negative correlation with overall survival of patients ( Bajkowska et al, 2020 ). Moreover, in breast cancer cells, overexpressed-NPTN contributes to tumor growth and angiogenesis in vivo , which is related to the increased VEGF production in microenvironmental hypoxia ( Rodriguez-Pinto et al, 2009 ).…”

Section: Main S100a8/a9-binding Receptors and Molecular Pathways In C...mentioning

confidence: 99%

The functions and regulatory pathways of S100A8/A9 and its receptors in cancers

Zhou,

Zhao,

Shao

et al. 2023

Front. Pharmacol.

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Inflammation primarily influences the initiation, progression, and deterioration of many human diseases, and immune cells are the principal forces that modulate the balance of inflammation by generating cytokines and chemokines to maintain physiological homeostasis or accelerate disease development. S100A8/A9, a heterodimer protein mainly generated by neutrophils, triggers many signal transduction pathways to mediate microtubule constitution and pathogen defense, as well as intricate procedures of cancer growth, metastasis, drug resistance, and prognosis. Its paired receptors, such as receptor for advanced glycation ends (RAGEs) and toll-like receptor 4 (TLR4), also have roles and effects within tumor cells, mainly involved with mitogen-activated protein kinases (MAPKs), NF-κB, phosphoinositide 3-kinase (PI3K)/Akt, mammalian target of rapamycin (mTOR) and protein kinase C (PKC) activation. In the clinical setting, S100A8/A9 and its receptors can be used complementarily as efficient biomarkers for cancer diagnosis and treatment. This review comprehensively summarizes the biological functions of S100A8/A9 and its various receptors in tumor cells, in order to provide new insights and strategies targeting S100A8/A9 to promote novel diagnostic and therapeutic methods in cancers.

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“…Moreover, over-expression of neuroplastin in a breast-cancerderived cell line strongly increased tumor growth and angiogenesis, as well as the production of vascular endothelia growth factor (VEGF), suggesting an angiogenic mechanism regulated by VEGF in the aberrant neuroplastin-expressing tumors [141]. Furthermore, the role of neuroplastin and its interaction with S100A8/A9, resulting in the activation of a cascade for lung cancer disseminative progression and aggressive development, has been proposed [142,143].…”

Section: Cancermentioning

confidence: 99%

Neuroplastin in Neuropsychiatric Diseases

Lin

Liang

Herrera-Molina

et al. 2021

Genes

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Molecular mechanisms underlying neuropsychiatric and neurodegenerative diseases are insufficiently elucidated. A detailed understanding of these mechanisms may help to further improve medical intervention. Recently, intellectual abilities, creativity, and amnesia have been associated with neuroplastin, a cell recognition glycoprotein of the immunoglobulin superfamily that participates in synapse formation and function and calcium signaling. Data from animal models suggest a role for neuroplastin in pathways affected in neuropsychiatric and neurodegenerative diseases. Neuroplastin loss or disruption of molecular pathways related to neuronal processes has been linked to various neurological diseases, including dementia, schizophrenia, and Alzheimer’s disease. Here, we review the molecular features of the cell recognition molecule neuroplastin, and its binding partners, which are related to neurological processes and involved in learning and memory. The emerging functions of neuroplastin may have implications for the treatment of diseases, particularly those of the nervous system.

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Neuroplastinβ-mediated upregulation of solute carrier family 22 member 18 antisense (SLC22A18AS) plays a crucial role in the epithelial-mesenchymal transition, leading to lung cancer cells' enhanced motility

Cited by 4 publications

References 36 publications

The Roles of Imprinted SLC22A18 and SLC22A18AS Gene Overexpression Caused by Promoter CpG Island Hypomethylation as Diagnostic and Prognostic Biomarkers for Non-Small Cell Lung Cancer Patients

The Roles of Imprinted SLC22A18 and SLC22A18AS Gene Overexpression Caused by Promoter CpG Island Hypomethylation as Diagnostic and Prognostic Biomarkers for Non-Small Cell Lung Cancer Patients

The functions and regulatory pathways of S100A8/A9 and its receptors in cancers

Neuroplastin in Neuropsychiatric Diseases

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