Expression and inactivation of osteopontin-degrading PHEX enzyme in squamous cell carcinoma

Neves, Raquel Leão; Chiarantin, Gabrielly M. Denadai; Nascimento, Fábio D.; Pesquero, João Bosco; Nader, Helena B.; Tersariol, Ivarne L.S.; McKee, Marc D.; Carmona, Adriana K.; Barros, Nilana M.T.

doi:10.1016/j.biocel.2016.05.016

Cited by 7 publications

(3 citation statements)

References 46 publications

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“…XLH is caused by inactivating mutations of the PHEX gene whose precise mechanism of action remains to be defined (Francis et al 1995;Jonsson et al 2003). Osteopontin was recently identified as the first protein substrate for PHEX, showing in the murine model of XLH (Hyp mice) an increase in osteopontin that contributes to the osteomalacia (Neves et al 2016).…”

Section: Normal Renal Functionmentioning

confidence: 99%

Biology of Fibroblast Growth Factor 23: From Physiology to Pathology

Courbebaisse

Lanske

2017

Cold Spring Harb Perspect Med

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Fibroblast growth factor (FGF)23 is a phosphaturic hormone produced by osteocytes and osteoblasts that binds to FGF receptors in the presence of the transmembrane protein αKlotho. FGF23 mainly targets the renal proximal tubule to inhibit calcitriol production and the expression of the sodium/phosphate cotransporters NaPi2a and NaPi2c, thus inhibiting renal phosphate reabsorption. FGF23 also acts on the parathyroid glands to inhibit parathyroid hormone synthesis and secretion. FGF23 regulation involves many systemic and local factors, among them calcitriol, phosphate, and parathyroid hormone. Increased FGF23 is primarily observed in rare acquired or genetic disorders, but chronic kidney disease is associated with a reactional increase in FGF23 to combat hyperphosphatemia. However, high FGF23 levels induce left ventricular hypertrophy (LVH) and are associated with an increased risk of mortality. In this review, we describe FGF23 physiology and the pathological consequences of high or low FGF23 levels.

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Section: Normal Renal Functionmentioning

confidence: 99%

Biology of Fibroblast Growth Factor 23: From Physiology to Pathology

Courbebaisse

Lanske

2017

Cold Spring Harb Perspect Med

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“…Hence, the higher transcription rates of SPP1 and PHEX in hOB-IC versus hOB-A in the present study point to a PHEX-OPN co-expression in hOB, which may be important to maintain the local equilibrium between osteoclastogenesis and ECM mineralization. Neves et al (2016) which demonstrated a PHEX-OPN co-expression and PHEX-mediated regulation of OPN function in squamous carcinoma cells support this assumption.…”

Section: Discussionmentioning

confidence: 60%

A matter of origin - identification of SEMA3A, BGLAP, SPP1 and PHEX as distinctive molecular features between bone site-specific human osteoblasts on transcription level

Zhang

Rau

Kotzagiorgis

et al. 2022

Front. Bioeng. Biotechnol.

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In oral and maxillofacial bone reconstruction, autografts from the iliac crest represent the gold standard due to their superior clinical performance, compared to autografts derived from other extraoral regions. Thus, the aim of our study was to identify putative differences between osteoblasts derived from alveolar (hOB-A) and iliac crest (hOB-IC) bone of the same donor (nine donors) by means of their molecular properties in 2D and 3D culture. We thereby focused on the gene expression of biomarkers involved in osteogenic differentiation, matrix formation and osteoclast modulation. Furthermore, we examined the transcriptional response to Vit.D3 in hOB-A and hOB-IC. Our results revealed different modulation modes of the biomarker expression in osteoblasts, namely cell origin/bone entity-dependent, and culture configuration- and/or time-dependent modulations. SEMA3A, SPP1, BGLAP and PHEX demonstrated the strongest dependence on cell origin. With respect to Vit.D3-effects, BGLAP, SPP1 and ALPL displayed the highest Vit.D3-responsiveness. In this context we demonstrated that the transcriptional Vit.D3-response concerning SPP1 and ALPL in human osteoblasts depended on the cell origin. The results indicate a higher bone remodeling activity of iliac crest than alveolar osteoblasts and support the growing evidence that a high osteoclast activity at the host-/donor bone interface may support graft integration.

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“…COMP was reported to promote fibrosis in multiple organs, such as the skin, lung, and liver, and also contributes to the development of tumors, including colon cancer, breast cancer, and hepatocellular carcinoma ( Li et al, 2018 ). A decrease in the PHEX activity leads to misregulation of osteopontin, which contributes to bone mineralization and is associated with metastasis in tumor biology ( Neves et al, 2016 ). MMP3 can be regulated by NFAT1 and promote melanoma tumor growth and lung metastasis ( Shoshan et al, 2016 ).…”

Section: Discussionmentioning

confidence: 99%

The Pathogenic Effects of Fusobacterium nucleatum on the Proliferation, Osteogenic Differentiation, and Transcriptome of Osteoblasts

Gao

Sun

Yang

et al. 2020

Front. Cell Dev. Biol.

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As one of the most common oral diseases, periodontitis is closely correlated with tooth loss in middle-aged and elderly people. Fusobacterium nucleatum ( F. nucleatum ) contributes to periodontitis, but the evidence in alveolar bone loss is still unclear. In this study, cytological experiments and transcriptome analyses were performed to characterize the biological process abnormalities and the molecular changes of F. nucleatum -stimulated osteoblasts. F. nucleatum could inhibit cell proliferation, promote cell apoptosis, and elevate pro-inflammatory cytokine production of osteoblasts, and it also inhibited osteoblast differentiation and mineralized nodule formation and decreased the expression of osteogenetic genes and proteins. Whole-transcriptome analyses identified a total of 235 transcripts that were differentially expressed in all six time points, most of which were inflammation-related genes. The genes, Ccl2 , Ccl20 , Csf1 , Cx3cl1 , Cxcl1 , Cxcl3 , Il6 , Birc3 , Map3k8 , Nos2 , Nfkb2 , Tnfrsf1b , and Vcam1 , played core roles in a PPI network, and interacted closely with other ones in the infection. In addition, 133 osteogenesis-related differential expression genes (DEGs) were time-serially dynamically changed in a short time-series expression miner (STEM) analysis, which were enriched in multiple cancer-related pathways. The core dynamic DEGs ( Mnda , Cyp1b1 , Comp , Phex , Mmp3 , Tnfrsf1b , Fbln5 , and Nfkb2 ) had been reported to be closely related to the development and metastasis in tumor and cancer progress. This study is the first to evaluate the long-term interaction of F. nucleatum on osteoblasts, which might increase the risk of cell carcinogenesis of normal osteoblasts, and provides new insight into the pathogenesis of bacterial-induced bone destruction.

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Expression and inactivation of osteopontin-degrading PHEX enzyme in squamous cell carcinoma

Cited by 7 publications

References 46 publications

Biology of Fibroblast Growth Factor 23: From Physiology to Pathology

Biology of Fibroblast Growth Factor 23: From Physiology to Pathology

A matter of origin - identification of SEMA3A, BGLAP, SPP1 and PHEX as distinctive molecular features between bone site-specific human osteoblasts on transcription level

The Pathogenic Effects of Fusobacterium nucleatum on the Proliferation, Osteogenic Differentiation, and Transcriptome of Osteoblasts

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