IGF-IR internalizes with CAVEOLIN-1 and PTRF/CAVIN in HACAT cells

Salani, Barbara; Passalacqua, Mario; Maffioli, Sara; Briatore, L.; Hamoudane, Meriem; Contini, Paola; Cordera, Renzo; Maggi, Davide

doi:10.1016/j.numecd.2013.10.009

Cited by 3 publications

(3 citation statements)

References 17 publications

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“…The alternative mechanisms may also involve several acceptor proteins known to mediate IgG internalization, such as clathrin, caveolin, megalin and cubilin [50]. While the former two proteins are known to be expressed in KCs [51], the expression of the latter two is unknown. The mechanism allowing PVIgGs to find their way to the mitochondrial targets is a subject of our current research.…”

Section: Discussionmentioning

confidence: 99%

Pemphigus vulgaris antibodies target the mitochondrial nicotinic acetylcholine receptors that protect keratinocytes from apoptolysis

Chernyavsky

Chen

Grando

2015

International Immunopharmacology

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Section: Discussionmentioning

confidence: 99%

Pemphigus vulgaris antibodies target the mitochondrial nicotinic acetylcholine receptors that protect keratinocytes from apoptolysis

Chernyavsky

Chen

Grando

2015

International Immunopharmacology

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“…In this context, the formation of Cavin-1 and Cav-1 complexes has been shown to promote a p53-dependent premature senescence in fibroblasts exposed to oxidative stress 102,103 and to regulate the internalization of IGF1R in human Hacat cells. 104,105 Hence, it will be important to assess whether Cavin-1 and Cav-1 complexes may influence specific targets, such as p53 and IGF1R, that play a central role in RMS progression. 17,106 It is also of interest that we found Cavin-1 colocalizing with Cav-2 in proliferating RMS cells.…”

Section: Discussionmentioning

confidence: 99%

Cavin-1 and Caveolin-1 are both required to support cell proliferation, migration and anchorage-independent cell growth in rhabdomyosarcoma

Faggi

Chiarelli

Colombi

et al. 2015

Laboratory Investigation

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Rhabdomyosarcoma (RMS) is a childhood soft tissue tumor with broad expression of markers that are typically found in skeletal muscle. Cavin-1 is a recently discovered protein actively cooperating with Caveolin-1 (Cav-1) in the morphogenesis of caveolae and whose role in cancer is drawing increasing attention. Using a combined in silico and in vitro analysis here we show that Cavin-1 is expressed in myogenic RMS tumors as well as in human and primary mouse RMS cultures, exhibiting a broad subcellular localization, ranging from nuclei and cytosol to plasma membrane. In particular, the coexpression and plasma membrane interaction between Cavin-1 and Cav-1 characterized the proliferation of human and mouse RMS cell cultures, while a downregulation of their expression levels was observed during the myogenic differentiation. Knockdown of Cavin-1 or Cav-1 in the human RD and RH30 cells led to impairment of cell proliferation and migration. Moreover, loss of Cavin-1 in RD cells impaired the anchorage-independent cell growth in soft agar. While the loss of Cavin-1 did not affect the Cav-1 protein levels in RMS cells, Cav-1 overexpression and knockdown triggered a rise or depletion of Cavin-1 protein levels in RD cells, respectively, in turn reflecting on increased or decreased cell proliferation, migration and anchorage-independent cell growth. Collectively, these data indicate that the interaction between Cavin-1 and Cav-1 underlies the cell growth and migration in myogenic tumors. Rhabdomyosarcoma (RMS) is a childhood soft tissue sarcoma exhibiting broad expression of skeletal muscle markers, 1-3 such as Pax7, MyoD, Myogenin, desmin and muscle-specific actin. 4,5 Cells of origin in RMS may be different muscular and non-muscular cell precursors, 6-8 such as muscle satellite cells (SCs), 9-11 and myoblasts 9,10,12-14 or adipocytes, 15 which are responsible of two major histological subtypes known as embryonal (ERMS) and alveolar (ARMS). The most common ERMS variant arises in children usually o5 years on distinct body sites, such as head, neck and genitourinary regions, while ARMS typically arises in the muscular limb extremities of adolescents and is characterized by poorer prognosis. 16 The genomic landscape causative of ERMS is characterized by a number of genetic lesions and/or somatic mutations that deliberately sustain the activity of different receptors, such as IGF1R, FGFR4 and Patched, 17-21 and related downstream pathways (i.e., RAS/ERK, PI3K/AKT and Sonic Hedgehog signaling). 11,22 In addition, defects in tumor suppressors (i.e., p53), 23 cell cycle regulatory genes (i.e., N-Myc, Rb1) 21,24 and structural proteins involved in muscular integrity (i.e., dystrophin, alpha-sarcoglycan and dysferlin) have been reported. [25][26][27][28][29][30] Conversely, ARMS is dominated by the presence of specific chromosomal translocations leading to expression of the fused Pax3-Foxo1 and Pax7-Foxo1 factors, that driving in a cell cycle manner the transcription of several genes normally restricted to the embryonal development f...

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“…The macropinocytosis-like endocytosis involving actin cytoskeleton rearrangements and membrane ruffling has been observed in early studies of epidermoid carcinoma A-431 cells that express very high levels of EGFR (Haigler et al 1979), and later in other cell types (Barbieri et al 2000;Yamazaki et al 2002;Orth et al 2006;Valdez et al 2007). Another mechanism implicated in the CIE of RTKs is defined by its sensitivity to inhibitors of caveolae and cholesterol-disrupting agents (Sigismund et al 2005;Sehat et al 2008;Salani et al 2010). However, the lack of experimental tools to inhibit specific CIE pathways impedes analysis of the mechanisms and functional role of CIE.…”

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confidence: 99%

Endocytosis of Receptor Tyrosine Kinases

Goh

Sorkin

2013

Cold Spring Harbor Perspectives in Biology

402

398

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Endocytosis is the major regulator of signaling from receptor tyrosine kinases (RTKs). The canonical model of RTK endocytosis involves rapid internalization of an RTK activated by ligand binding at the cell surface and subsequent sorting of internalized ligand-RTK complexes to lysosomes for degradation. Activation of the intrinsic tyrosine kinase activity of RTKs results in autophosphorylation, which is mechanistically coupled to the recruitment of adaptor proteins and conjugation of ubiquitin to RTKs. Ubiquitination serves to mediate interactions of RTKs with sorting machineries both at the cell surface and on endosomes. The pathways and kinetics of RTK endocytic trafficking, molecular mechanisms underlying sorting processes, and examples of deviations from the standard trafficking itinerary in the RTK family are discussed in this work.F unctional activities of transmembrane proteins, including the large family of RTKs, are controlled by intracellular trafficking. RTKs are synthesized in the endoplasmic reticulum, transported to Golgi apparatus, and then delivered to the plasma membrane. At the cell surface RTKs undergo constitutive endocytosis (internalization) at a rate similar to that of other integral membrane proteins. Constitutive internalization of RTKs is much slower than their constitutive recycling from endosomes back to the cell surface. Therefore, RTKs are accumulated at the cell surface, which allows maximal accessibility to extracellular ligands. The rates of the constitutive internalization, recycling, and degradation determine the half-life of an RTK protein, which varies depending on the nature of the RTK and the cell type, and typically positively correlates with the expression level of the RTK. For example, the turnover rates range from t 1/2 ,

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IGF-IR internalizes with CAVEOLIN-1 and PTRF/CAVIN in HACAT cells

Cited by 3 publications

References 17 publications

Pemphigus vulgaris antibodies target the mitochondrial nicotinic acetylcholine receptors that protect keratinocytes from apoptolysis

Pemphigus vulgaris antibodies target the mitochondrial nicotinic acetylcholine receptors that protect keratinocytes from apoptolysis

Cavin-1 and Caveolin-1 are both required to support cell proliferation, migration and anchorage-independent cell growth in rhabdomyosarcoma

Endocytosis of Receptor Tyrosine Kinases

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