PEBP1/RKIP behavior: a mirror of actin-membrane organization

Schoentgen, Françoise; Jonić, Slavica

doi:10.1007/s00018-020-03455-5

Cited by 22 publications

(23 citation statements)

References 108 publications

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“…In a previous study on pork Longissimus muscle, we found negative correlations between PEBP1 and L* and a* values (Kwasiborski et al 2008). The role of PEBP1 in determining beef colour may also be related to its interactions with many multifunctional proteins and involvement in the coordination of cytoskeleton changes and energy metabolism (Schoentgen & Jonic 2020). This is also consistent with the observed relationship between PEPB1 and energy metabolism (Figure 3A,B).…”

Section: Capn1 and Pebp1 As Protein Biomarkers Of Beef Coloursupporting

confidence: 90%

Proteomic biomarkers of beef colour

Gagaoua

Hughes²,

Terlouw³

et al. 2020

Trends in Food Science & Technology

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Section: Capn1 and Pebp1 As Protein Biomarkers Of Beef Coloursupporting

confidence: 90%

Proteomic biomarkers of beef colour

Gagaoua

Hughes²,

Terlouw³

et al. 2020

Trends in Food Science & Technology

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“…In this sense, and despite the described role for RKIP in the regulation of the MAPK/ERK pathway, RKIP has been implicated on the invasive behavior of malignant melanoma cells but not on their proliferative capability [14]. Moreover, Schoentgen and Jonic [16] described the involvement of RKIP on the cortical actin organization during the membrane changes that happen during tumor cell migration. In agreement with previous studies, we confirmed the implication of RKIP on the motility of malignant melanoma cells as RKIP expression was inversely correlated with the migration capability of both, primary and metastatic melanoma cell lines.…”

Section: Discussionmentioning

confidence: 99%

“…Malignant transformation of cells implies the acquisition of particular characteristics in terms of survival and proliferative capability, while metastatic spreading depends on enhanced migration and invasion [16]. In addition, tumor persistence seems to rely on a particular subset of cells with acquired "stem cell-like" properties [17,18].…”

Section: Introductionmentioning

confidence: 99%

RKIP Regulates Differentiation-Related Features in Melanocytic Cells

Penas

Apraiz

Muñoa

et al. 2020

Cancers

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Raf Kinase Inhibitor Protein (RKIP) has been extensively reported as an inhibitor of key signaling pathways involved in the aggressive tumor phenotype and shows decreased expression in several types of cancers. However, little is known about RKIP in melanoma or regarding its function in normal cells. We examined the role of RKIP in both primary melanocytes and malignant melanoma cells and evaluated its diagnostic and prognostic value. IHC analysis revealed a significantly higher expression of RKIP in nevi compared with early-stage (stage I–II, AJCC 8th) melanoma biopsies. Proliferation, wound healing, and collagen-coated transwell assays uncovered the implication of RKIP on the motility but not on the proliferative capacity of melanoma cells as RKIP protein levels were inversely correlated with the migration capacity of both primary and metastatic melanoma cells but did not alter other parameters. As shown by RNA sequencing, endogenous RKIP knockdown in primary melanocytes triggered the deregulation of cellular differentiation-related processes, including genes (i.e., ZEB1, THY-1) closely related to the EMT. Interestingly, NANOG was identified as a putative transcriptional regulator of many of the deregulated genes, and RKIP was able to decrease the activation of the NANOG promoter. As a whole, our data support the utility of RKIP as a diagnostic marker for early-stage melanomas. In addition, these findings indicate its participation in the maintenance of a differentiated state of melanocytic cells by modulating genes intimately linked to the cellular motility and explain the progressive decrease of RKIP often described in tumors.

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“…Phosphatidylethanolamine-binding protein 1 (PEBP1), which is also referred to as Raf1 kinase inhibitory protein (RKIP), has been found to be potentially involved in diverse biological functions through the regulation of various protein kinases in several signaling pathways, such as the RAF/MEK/mitogen-activated protein kinase (MAPK)/extracellular regulated kinase (ERK), nuclear factor (NF)-κB and PI3K/Akt/mammalian target of rapamycin (mTOR) pathways (25,26). In addition, the influence of PEBP1 on cell apoptosis, proliferation, migration and autophagy has been demonstrated.…”

Section: Introductionmentioning

confidence: 99%

LINC00473 rescues human bone marrow mesenchymal stem cells from apoptosis induced by dexamethasone through the PEBP1‑mediated Akt/Bad/Bcl‑2 signaling pathway

Jiang

Wang

et al. 2020

Int J Mol Med

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The inhibition of the proliferation and apoptosis of bone marrow-derived mesenchymal stem cells (BMSCs) triggered by the excessive use of glucocorticoids, is considered a potential mechanism for the pathogenesis of steroid-induced osteonecrosis of the femoral head (SONFH). Long non-coding RNAs (lncRNAs) have been proven to influence the proliferation, apoptosis and differentiation of BMSCs by regulating the expression of critical genes. A previous microarray analysis by the authors confirmed the significant downregulation of LINC00473 in human BMSCs (hBMSCs) from patients with SONFH. However, the underlying role and molecular mechanisms of LINC00473 on dexamethasone (Dex)-stimulated hBMSCs remains unknown. In the present study, the expression of LINC00473 was determined in the hBMSCs of patients with SONFH and control patients. In addition, the protective effects and underlying molecular mechanisms of LINC00473 in Dex-stimulated hBMSCs were investigated. The results revealed that LINC00473 expression was significantly down-regulated in hBMSCs from patients with SONFH compared with the controls, and that the upregulation of LINC00473 attenuated the inhibitory effects exerted by 1 µ M Dex on the proliferation and apoptosis of hBMSCs. Moreover, the upregulation of LINC00473 significantly promoted the protein expression of phosphorylated (p-)Akt, p-Bcl-2-associated death promoter (p-Bad) and B-cell lymphoma 2 (Bcl-2), whereas it decreased the cleavage of caspase-3, thus preventing the Dex-induced apoptosis of hBMSCs. Of note, the regulatory effects of LINC00473 on the Akt/Bad/Bcl-2 signaling pathway and its anti-apoptotic effects were similar to those of SC79 (an Akt activator), and were inhibited by MK-2206 (an Akt inhibitor). In further experiments, it was found that the upregulation of LINC00473 markedly promoted the phosphorylation of Akt in Dex-stimulated hBMSCs, and increased the protein level of phosphatidylethanolamine-binding protein 1 (PEBP1). Alternatively, the promoting effect on Akt phosphorylation induced by LINC00473 was significantly attenuated following the knockdown of PEBP1. Furthermore, the upregulation of PEBP1 triggered a marked increase in the levels of Akt phosphorylation in Dex-stimulated hBMSCs, which was line with the upregulation of LINC00473. Taken together, the results of the present study demonstrate that LINC00473 has the ability to rescue hBMSCs from Dex-induced apoptosis through the PEBP1-mediated activation of the Akt/Bad/Bcl-2 signaling pathway.

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PEBP1/RKIP behavior: a mirror of actin-membrane organization

Cited by 22 publications

References 108 publications

Proteomic biomarkers of beef colour

Proteomic biomarkers of beef colour

RKIP Regulates Differentiation-Related Features in Melanocytic Cells

LINC00473 rescues human bone marrow mesenchymal stem cells from apoptosis induced by dexamethasone through the PEBP1‑mediated Akt/Bad/Bcl‑2 signaling pathway

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