Understanding the Role of the BAI Subfamily of Adhesion G Protein-Coupled Receptors (GPCRs) in Pathological and Physiological Conditions

Moon, Sun Young; Shin, Seong-Ah; Oh, Yong‐Seok; Park, Hyun Ho; Lee, Chang Sup

doi:10.3390/genes9120597

Cited by 13 publications

(8 citation statements)

References 85 publications

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“…For example, mutation of BAI3 is found to be dramatically enriched in the micropapillary tumors of European patients, but not in Asian patients. BAI3 is a member of the adhesion G protein-coupled receptor and it has been shown to be involved in diverse physiological and pathological conditions, including myoblast fusion, tumor progression, and neurological diseases (32). BAI3 was found to be upregulated in small-cell lung cancer, although its function in these tumors was still unclear (33).…”

Section: Discussionmentioning

confidence: 99%

Integrated Analysis of Genomic and Immunological Features in Lung Adenocarcinoma With Micropapillary Component

Zhang

Xu²,

Zhao

et al. 2021

Front. Oncol.

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BackgroundMicropapillary adenocarcinoma is one of the most aggressive histologic subtypes of lung adenocarcinoma (LADC), and even a minor proportion of micropapillary component (MPC) within the LADC could contribute to poor prognosis. Comprehensive analysis of genetic and immunological features of LADC with different percentages of MPC would help better understand cancer biology of this LADC subtype and direct future treatments.MethodsWe performed next-generation sequencing (NGS) for a discovery cohort of 43 LADC patients whose tumors were micro-dissected to separate MPC and non-MPC lesions and a reference cohort of 113 LADC patients. MPC-enriched genetic alterations that were detected in the discovery cohort were then confirmed using a validation cohort of 183 LADC patients. Immunological staining was also conducted on the MPC-containing samples in the discovery cohort.ResultsTumors with a higher percentage of MPC tended to harbor more tumor mutation burdens (TMBs) and chromosome instability (CIN). Some rare genetic events may serve as the genetic landscape to drive micropapillary tumor progression. Specifically, alterations in transcription termination factor 1 (TTF1), brain-specific angiogenesis inhibitor 3 (BAI3), mammalian target of rapamycin (MTOR), and cyclin-dependent kinase inhibitor 2A (CDKN2A) were cross-validated to be enriched in MPC-contained LADC. Additionally, tumors with a higher percentage of MPC were associated with a higher percentage of CD4+, CD8+, and PD-L1+ staining, and some genetic changes that were enriched in MPC, including MET amplification and MTOR mutation, were correlated with increased PD-L1 expression.ConclusionWe identified multiple novel MPC-enriched genetic changes that could help us understand the nature of this aggressive cancer subtype. High MPC tumors tended to have elevated levels of TMBs, T cell infiltration, and immunosuppression than low MPC tumors, implying the potential link between MPC content and sensitivity to immunotherapy.

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Section: Discussionmentioning

confidence: 99%

Integrated Analysis of Genomic and Immunological Features in Lung Adenocarcinoma With Micropapillary Component

Zhang

Xu²,

Zhao

et al. 2021

Front. Oncol.

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“…The process of phagocytosis is essential for clearance of dead cells, microorganisms and other foreign material [27]. Lack of clearance of apoptotic cells may lead to necrosis, autoimmunity and chronic inflammation [28][29][30][31]. Three categories of phagocytic cells have been described [32].…”

Section: Discussionmentioning

confidence: 99%

Myo/Nog cells are nonprofessional phagocytes

et al. 2020

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Myo/Nog cells were discovered in the chick embryo epiblast. Their expression of MyoD reflects a commitment to the skeletal muscle lineage and capacity to differentiate into myofibroblasts. Release of Noggin by Myo/Nog cells is essential for normal morphogenesis. Myo/ Nog cells rapidly respond to wounding in the skin and eyes. In this report, we present evidence suggesting that Myo/Nog cells phagocytose tattoo ink in tissue sections of human skin and engulf cell corpses in cultures of anterior human lens tissue and magnetic beads injected into the anterior chamber of mice in vivo. Myo/Nog cells are distinct from macrophages in the skin and eyes indicated by the absence of labeling with an antibody to ionized calcium binding adaptor molecule 1. In addition to their primary roles as regulators of BMP signaling and progenitors of myofibroblasts, Myo/Nog cells behave as nonprofessional phagocytes defined as cells whose primary functions are unrelated to phagocytosis but are capable of engulfment.

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“… P4-ATPases of the ATP 8, 9, 10, and 11 families Flip PS from the exofacial to the cytofacial leaflet of the PM ( 61 ) Myoblasts ( 169 ) ABC transporter CED-7 Elicits PS exposure on axon PMs in C. elegans ( 194 ) Axon regeneration ( 127 ) PLSCRs May play some role in eliciting PS exposure ( 79 , 81 ) Viral entry ( 82 ) PS recognizing machinery Annexins Soluble, PS-binding proteins that function as assembly factors in many biological processes ( 195 ) Myoblasts ( 21 , 196 ), trophoblasts ( 167 ), osteoclasts ( 22 ) Lactadherin Soluble, PS-binding protein ( 197 ) Sperm-egg ( 168 ) Protein S Soluble, PS-binding protein ( 198 ) ? GAS-6 Soluble, PS-binding protein ( 177 ) Viral entry ( 199 ) CD300 receptors Membrane-bound receptors with affinity for exofacial lipids, some specifically bind PS ( 200 ) Viral entry ( 201 ) TIM receptors 1 and 4 Membrane-bound PS receptors with major roles in immunity ( 202 ) Viral entry ( 203 ) BAI receptors 1 and 3 Membrane-bound PS receptors ( 204 ) Myoblasts ( 162 ) Stabilin 2 Membrane-bound PS receptor ( 205 ) Myoblasts ( ...…”

Section: Regulation Of the Membrane-remodeling Stages Of Cell Fusionmentioning

confidence: 99%

Flagging fusion: Phosphatidylserine signaling in cell–cell fusion

Whitlock

Chernomordik

2021

Journal of Biological Chemistry

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Formations of myofibers, osteoclasts, syncytiotrophoblasts, and fertilized zygotes share a common step, cell–cell fusion. Recent years have brought about considerable progress in identifying some of the proteins involved in these and other cell-fusion processes. However, even for the best-characterized cell fusions, we still do not know the mechanisms that regulate the timing of cell-fusion events. Are they fully controlled by the expression of fusogenic proteins or do they also depend on some triggering signal that activates these proteins? The latter scenario would be analogous to the mechanisms that control the timing of exocytosis initiated by Ca 2+ influx and virus-cell fusion initiated by low pH- or receptor interaction. Diverse cell fusions are accompanied by the nonapoptotic exposure of phosphatidylserine at the surface of fusing cells. Here we review data on the dependence of membrane remodeling in cell fusion on phosphatidylserine and phosphatidylserine-recognizing proteins and discuss the hypothesis that cell surface phosphatidylserine serves as a conserved “fuse me” signal regulating the time and place of cell-fusion processes.

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Understanding the Role of the BAI Subfamily of Adhesion G Protein-Coupled Receptors (GPCRs) in Pathological and Physiological Conditions

Cited by 13 publications

References 85 publications

Integrated Analysis of Genomic and Immunological Features in Lung Adenocarcinoma With Micropapillary Component

Integrated Analysis of Genomic and Immunological Features in Lung Adenocarcinoma With Micropapillary Component

Myo/Nog cells are nonprofessional phagocytes

Flagging fusion: Phosphatidylserine signaling in cell–cell fusion

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