Adhesion GPCRs in Tumorigenesis

Aust, Gabriela; Zhu, Da‐Yuan; Eg, Van Meir; Xu, Lian

doi:10.1007/978-3-319-41523-9_17

Cited by 62 publications

(59 citation statements)

References 157 publications

(201 reference statements)

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“…aGPCRs are known to modulate pivotal cellular functions including migration, adhesion, polarity and guidance ( 4 ). Consistently, members from all aGPCR subfamilies have been reported in the context of dysplasia and tumorigenesis in one way or another ( 5 – 8 ). While for some receptors it is mere evidence of faulty expression or changes in their activity (e.g., VLGR1/ADGRV, LPHN/ADGRL), for others more detailed knowledge about the molecular mechanisms that make cells or tissues go awry have emerged [e.g., CD97/ADGRE5 ( 9 – 11 ), GPR116/ADGRF5 ( 12 , 13 ), GPR133/ADGRD1 ( 14 , 15 ), GPR56/ADGRG1 ( 16 – 19 ), and BAI1/ADRGB1 ( 20 – 22 )].…”

Section: Introductionsupporting

confidence: 53%

Cancer Cell Mechanics: Adhesion G Protein-coupled Receptors in Action?

Scholz

2018

Front. Oncol.

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In mammals, numerous organ systems are equipped with adhesion G protein-coupled receptors (aGPCRs) to shape cellular processes including migration, adhesion, polarity and guidance. All of these cell biological aspects are closely associated with tumor cell biology. Consistently, aberrant expression or malfunction of aGPCRs has been associated with dysplasia and tumorigenesis. Mounting evidence indicates that cancer cells comprise viscoelastic properties that are different from that of their non-tumorigenic counterparts, a feature that is believed to contribute to the increased motility and invasiveness of metastatic cancer cells. This is particularly interesting in light of the recent identification of the mechanosensitive facility of aGPCRs. aGPCRs are signified by large extracellular domains (ECDs) with adhesive properties, which promote the engagement with insoluble ligands. This configuration may enable reliable force transmission to the ECDs and may constitute a molecular switch, vital for mechano-dependent aGPCR signaling. The investigation of aGPCR function in mechanosensation is still in its infancy and has been largely restricted to physiological contexts. It remains to be elucidated if and how aGPCR function affects the mechanoregulation of tumor cells, how this may shape the mechanical signature and ultimately determines the pathological features of a cancer cell. This article aims to view known aGPCR functions from a biomechanical perspective and to delineate how this might impinge on the mechanobiology of cancer cells.

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Section: Introductionsupporting

confidence: 53%

Cancer Cell Mechanics: Adhesion G Protein-coupled Receptors in Action?

Scholz

2018

Front. Oncol.

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“…Only few and sometimes contradictory expression data on latrophilins in tumors and tumor cell lines are available (Aust 2010). However, interesting results regarding the function of LPHN1 in the etiopathogenesis of AML were published in 2017.…”

Section: Resultsmentioning

confidence: 99%

Overexpression of the ABCB1 drug transporter in acute myeloid leukemia cells is associated with downregulation of latrophilin-1

Kocibalova¹,

Guzyova²,

Imrichova³

et al. 2018

gpb

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Finding new markers with appropriate prognostic levels for the differential diagnosis of neoplastic diseases represents an important issue for biomedical research. Recently, latrophilin-1 (LPHN1) was reported to be expressed in human monocytic leukemia cell lines and in primary human acute myeloid leukemia (AML) cells. However, this expression was found to be absent in healthy leukocytes. LPHN1 was therefore considered a novel biomarker of human AML. In previous papers, we established two P-gp-positive variants (SKM-1/VCR and MOLM-13/VCR) of AML cell lines derived from parental human AML cells SKM-1 and MOLM-13 by selection with VCR. The present paper addresses the measurement of LPHN1 expression in SKM-1 and MOLM-13 cells and their P-gp-positive variants. Both parental AML lines were positive for LPHN1 expression at the mRNA and protein levels. However, the expression of LPHN1 at both the mRNA and protein levels was reduced in both P-gp-positive SKM-1/VCR and MOLM-13/VCR variants of AML cells. Interestingly, we observed an elevation of the latrophilin-3 transcript in P-gp-positive variants of AML cell lines. The combined results suggest that alterations in latrophilin expression occur in AML cells expressing P-gp.

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“…Surface proteins and receptors involved in immune response and immunomodulation were also highly present on SH-SY5Y cells (CD46, CD47, CD59, CD197, CD200) 43 – 46 . Other highly expressed markers play roles in nutrient uptake (CD71, CD220) 47 , 48 , detection of mitogenic as well as apoptotic signals (CD140A, CD140B, CD221) 49 , migration of neural crest cells during embryological development (CD184) 50 – 53 or are strongly associated with tumor invasion (CD56, CD97, CD146, CD147, CD166) 41 , 54 , 55 . Also, factors critical for normal neurohistogenesis (CD171) 26 , 56 , metastasis of NB (CD44) 27 , 57 and modulation of CD184 expression (CD13) 58 were identified with expression levels >50% on the NB cells.…”

Section: Resultsmentioning

confidence: 99%

Surface marker profiling of SH-SY5Y cells enables small molecule screens identifying BMP4 as a modulator of neuroblastoma differentiation

Ferlemann

Menon

Condurat

et al. 2017

Sci Rep

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Neuroblastoma is the most common extra-cranial solid tumor in children. Its broad spectrum of clinical outcomes reflects the underlying inherent cellular heterogeneity. As current treatments often do not lead to tumor eradication, there is a need to better define therapy-resistant neuroblastoma and to identify new modulatory molecules. To this end, we performed the first comprehensive flow cytometric characterization of surface molecule expression in neuroblastoma cell lines. Exploiting an established clustering algorithm (SPADE) for unbiased visualization of cellular subsets, we conducted a multiwell screen for small molecule modulators of neuroblastoma phenotype. In addition to SH-SY5Y cells, the SH-EP, BE(2)-M17 and Kelly lines were included in follow-up analysis as in vitro models of neuroblastoma. A combinatorial detection of glycoprotein epitopes (CD15, CD24, CD44, CD57, TrkA) and the chemokine receptor CXCR4 (CD184) enabled the quantitative identification of SPADE-defined clusters differentially responding to small molecules. Exposure to bone morphogenetic protein (BMP)-4 was found to enhance a TrkAhigh/CD15−/CD184− neuroblastoma cellular subset, accompanied by a reduction in doublecortin-positive neuroblasts and of NMYC protein expression in SH-SY5Y cells. Beyond yielding novel marker candidates for studying neuroblastoma pathology, our approach may provide tools for improved pharmacological screens towards developing novel avenues of neuroblastoma diagnosis and treatment.

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Adhesion GPCRs in Tumorigenesis

Cited by 62 publications

References 157 publications

Cancer Cell Mechanics: Adhesion G Protein-coupled Receptors in Action?

Cancer Cell Mechanics: Adhesion G Protein-coupled Receptors in Action?

Overexpression of the ABCB1 drug transporter in acute myeloid leukemia cells is associated with downregulation of latrophilin-1

Surface marker profiling of SH-SY5Y cells enables small molecule screens identifying BMP4 as a modulator of neuroblastoma differentiation

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