Pathologic Caveolin-1 Regulation Of PTEN In Idiopathic Pulmonary Fibrosis

Xia, Hong; Khalil, Wajahat; Kahm, Judy; Jessurun, José; Kleidon, Jill; Henke, Craig A.

doi:10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3507

Cited by 34 publications

(58 citation statements)

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“…Interestingly, PI3K has been found in caveolae fractions in different cells, including fibroblasts, endothelial cells, and myeloid-derived cells [96] and, consistent with a role as a tumor suppressor, Caveolin-1 has been suggested to inhibit PI3K activity [97]. In a cellular context, this may also involve stabilizing the tumor suppressor phosphatase PTEN [98].…”

Section: The Pi3k/akt Connectionmentioning

confidence: 97%

“…Many of these interactions, such as those with the epidermal growth factor receptor, Src kinases, the Ras/Raf/MAPK pathway, PKCs and endothelial nitric oxide synthase (eNOS), occur via the scaffolding domain of Caveolin-1 (CSD; amino acids [82][83][84][85][86][87][88][89][90][91][92][93][94][95][96][97][98][99][100][101] and the scaffolding domain binding domain (CBD) found in the respective target proteins [3]. However, as highlighted in Fig.…”

Section: Caveolin-1-mediated Control In Signalingmentioning

confidence: 99%

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The Caveolin-1 Connection to Cell Death and Survival

Quest

Lobos-González²,

Núñez³

et al. 2013

Current Molecular Medicine

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Abstract:Caveolins are a family of membrane proteins required for the formation of small plasma membrane invaginations called caveolae that are implicated in cellular trafficking processes. In addition to this structural role, these scaffolding proteins modulate numerous intracellular signaling pathways; often via direct interaction with specific binding partners. Caveolin-1 is particularly well-studied in this respect and has been attributed a large variety of functions. Thus, Caveolin-1 also represents the best-characterized isoform of this family with respect to its participation in cancer. Rather strikingly, available evidence indicates that Caveolin-1 belongs to a select group of proteins that function, depending on the cellular settings, both as tumor suppressor and promoter of cellular traits commonly associated with enhanced malignant behavior, such as metastasis and multi-drug resistance. The mechanisms underlying such ambiguity in Caveolin-1 function constitute an area of great interest. Here, we will focus on discussing how Caveolin-1 modulates cell death and survival pathways and how this may contribute to a better understanding of the ambiguous role this protein plays in cancer.

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Section: The Pi3k/akt Connectionmentioning

confidence: 97%

Section: Caveolin-1-mediated Control In Signalingmentioning

confidence: 99%

The Caveolin-1 Connection to Cell Death and Survival

Quest

Lobos-González²,

Núñez³

et al. 2013

Current Molecular Medicine

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“…This is indicated by several studies showing that enhanced growth factor signalling, e.g. by deletion of the main AKT-inhibiting phosphatase PTEN, not only drives fibroproliferation, but also regulates myofibroblast differentiation and integrity of alveolar epithelial cells [248][249][250][251].…”

Section: Dysregulated Nutrient Sensingmentioning

confidence: 99%

Hallmarks of the ageing lung

2015

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Ageing is the main risk factor for major non-communicable chronic lung diseases, including chronic obstructive pulmonary disease, most forms of lung cancer and idiopathic pulmonary fibrosis. While the prevalence of these diseases continually increases with age, their respective incidence peaks at different times during the lifespan, suggesting specific effects of ageing on the onset and/or pathogenesis of chronic obstructive pulmonary disease, lung cancer and idiopathic pulmonary fibrosis. Recently, the nine hallmarks of ageing have been defined as cell-autonomous and non-autonomous pathways involved in ageing. Here, we review the available evidence for the involvement of each of these hallmarks in the pathogenesis of chronic obstructive pulmonary disease, lung cancer, or idiopathic pulmonary fibrosis. Importantly, we propose an additional hallmark, "dysregulation of the extracellular matrix", which we argue acts as a crucial modifier of cell-autonomous changes and functions, and as a key feature of the above-mentioned lung diseases. @ERSpublications Hallmarks of ageing are selecting factors for the pathogenesis of COPD, lung cancer and IPF

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“…Since Cav-1 contains sequences for PTEN binding (Xia et al 2010), the up-or down-regulation of Cav-1 expression, in turn, increases or decreased membrane content of PTEN. PTEN is a lipid/protein phosphatase, which induces dephosphorylation and inhibition of PI3K (Robbins and Hague 2016).…”

Section: Page 10 Of 27 Psychopharmacologymentioning

confidence: 99%

“…Phosphatase and tensin homologue (PTEN) inhibits PI3K/AKT pathway by dephosphorylation of PI3K (Robbins and Hague 2016); whereas caveolae protein, caveolin 1 (Cav-1) that binds directly to PTEN, regulates membrane content and function of the latter (Xia et al 2010). Caveolae are small lipid rafts of the plasma membrane which contribute to cell signalling (Sowa 2011).…”

Section: Introductionmentioning

confidence: 99%

Bi-phasic regulation of glycogen content in astrocytes via Cav-1/PTEN/PI3K/AKT/GSK-3β pathway by fluoxetine

Bai

Song

et al. 2017

Psychopharmacology

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Here we present the data indicating that chronic treatment with fluoxetine regulates Cav-1/PTEN/PI3K/AKT/GSK-3β signalling pathway and glycogen content in primary cultures of astrocytes with bi-phasic concentration dependence. At lower concentrations fluoxetine down-regulates gene expression of Cav-1, decreases membrane content of PTEN, increases activity of PI3K/AKT, and elevates GSK-3β phosphorylation thus suppressing its activity. At higher concentrations fluoxetine acts in an inverse fashion. As expected, fluoxetine at lower concentrations increased while at higher concentrations decreased glycogen content in astrocytes. Our findings indicate that bi-phasic regulation of glycogen content via Cav-1/PTEN/AKT/GSK-3β pathway by fluoxetine may be responsible for both therapeutic and side effects of the drug.

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Pathologic Caveolin-1 Regulation Of PTEN In Idiopathic Pulmonary Fibrosis

Cited by 34 publications

References 0 publications

The Caveolin-1 Connection to Cell Death and Survival

The Caveolin-1 Connection to Cell Death and Survival

Hallmarks of the ageing lung

Bi-phasic regulation of glycogen content in astrocytes via Cav-1/PTEN/PI3K/AKT/GSK-3β pathway by fluoxetine

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