Keeping in touch with the membrane; protein- and lipid-mediated confinement of caveolae to the cell surface

Hubert, Madlen; Larsson, Elin; Lundmark, Richard

doi:10.1042/bst20190386

Cited by 40 publications

(26 citation statements)

References 71 publications

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“…Of note, caveola formation or stability is assisted by other proteins implicated in cancer, such as PACSINs [106,146] and EHDs [84,110]. A detailed discussion of these proteins and their participation in related processes is however beyond the scope of this review and can be found elsewhere [58,66,91,131,149].…”

Section: Role Of Cav1 In Migrationmentioning

confidence: 99%

Caveolin-1 function at the plasma membrane and in intracellular compartments in cancer

Simón

Campos

Leyton

et al. 2020

Cancer Metastasis Rev

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Caveolin-1 (CAV1) is commonly considered to function as a cell surface protein, for instance in the genesis of caveolae. Nonetheless, it is also present in many intracellular organelles and compartments. The contributions of these intracellular pools to CAV1 function are generally less well understood, and this is also the case in the context of cancer. This review will summarize literature available on the role of CAV1 in cancer, highlighting particularly our understanding of the canonical (CAV1 in the plasma membrane) and non-canonical pathways (CAV1 in organelles and exosomes) linked to the dual role of the protein as a tumor suppressor and promoter of metastasis. With this in mind, we will focus on recently emerging concepts linking CAV1 function to the regulation of intracellular organelle communication within the same cell where CAV1 is expressed. However, we now know that CAV1 can be released from cells in exosomes and generate systemic effects. Thus, we will also elaborate on how CAV1 participates in intracellular communication between organelles as well as signaling between cells (non-canonical pathways) in cancer.

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Section: Role Of Cav1 In Migrationmentioning

confidence: 99%

Caveolin-1 function at the plasma membrane and in intracellular compartments in cancer

Simón

Campos

Leyton

et al. 2020

Cancer Metastasis Rev

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“…As a structural component of caveolae, caveolin-1 exerts crucial function in a variety of cellular functions, consisting of cell growth, adhesion, signal transduction, migration, senescence, development, and tumorigenesis (Boscher and Nabi, 2012;Ketteler and Klein, 2018;Volonte and Galbiati, 2020). Caveolin-1 also played an important role in mechanosensing that reflects the response the mechanical forces (extracellular matrix stiffness, vascular shear stress, and muscle stretching) reaching on the plasma membrane and affects the membrane integrity and repair (Dewulf et al, 2019;Del Pozo et al, 2020;Hubert et al, 2020;Liu, 2020;Singh and Lamaze, 2020). Caveolin 1 involves in the EMT in lung cancer (Garnett, 2016;Shi et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

Lentinan Attenuated the PM2.5 Exposure-Induced Inflammatory Response, Epithelial–Mesenchymal Transition and Migration by Inhibiting the PVT1/miR-199a-5p/caveolin1 Pathway in Lung Cancer

Liu

Wang

et al. 2021

DNA and Cell Biology

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PM2.5 plays an important role in the physiological and pathological progression of lung cancer. Lentinan exerts antitumor activity in many kinds of human cancers. Plasmacytoma variant translocation 1 (PVT1) exerts antitumor activity in many kinds of human cancers. However, the role and underlying molecular mechanism of PVT1 in the role of lentinan in PM2.5-exposed lung cancer are still largely unknown. Our study confirmed that PM2.5 exposure induced the production of inflammatory factors, epithelial-mesenchymal transition (EMT) and migration of lung cancer cells. Lentinan exerted antitumor effects by inhibiting the production of inflammatory factors, EMT, and migration of lung cancer cells. Lentinan suppressed PM2.5 exposure-induced cellular progression by inhibiting the PM2.5 exposure-induced elevation of PVT1 expression. PVT1 absorbed miR-199a, and miR-199a inhibited caveolin1 expression and thus formed the PVT1/miR-199a/caveolin1 signaling pathway in lung cancer cells. Our study revealed that silencing of the PVT1/miR-199a/caveolin1 signaling pathway affected the role of lentinan in PM2.5-exposed lung cancer cells. Thus, this study first investigated the role of lentinan in PM2.5-exposed lung cancer cells and further displayed the underlying molecular mechanism, providing a potential treatment for PM2.5-exposed lung cancer.

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“…GSN (Silacci et al, 2004) regulates the formation of the actin skeleton by assembling or dissembling actin filaments and forming molecular complexes that rapidly dissociate and reform to accomplish actin remodeling. PACSIN2 is a membrane sculpting protein (Hubert et al, 2020) known to play an important and unique role in megakaryocyte membrane invagination (Begonja et al, 2015;Chitu and Stanley, 2015) and impact platelet formation and function. CELF2 (Barreau et al, 2006) and MBNL1 (Meola et al, 2013) are RNA-binding proteins, with recognized roles in mRNA splicing; and their epigenetic loss associated with aberrant growth inhibition and poor clinical outcome in other cancers (Pique et al, 2019).…”

Section: Increasing Alternative Splicing Of Genes That Are Also Differentially Expressed Confirm Increasingly Impaired Proteostasis By Mpmentioning

confidence: 99%

Platelet transcriptome yields progressive markers in chronic myeloproliferative neoplasms and identifies putative targets of therapy

Shen

Perkins

et al. 2021

Preprint

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Predicting disease natural history remains a particularly challenging endeavor in chronic degenerative disorders and cancer, thus limiting early detection, risk stratification, and preventive interventions. Here, profiling the spectrum of chronic myeloproliferative neoplasms (MPNs), as a model, we identify the blood platelet transcriptome as a generalizable strategy for highly sensitive progression biomarkers that also enable prediction via machine learning algorithms. Using RNA sequencing (RNA seq), we derive disease relevant gene expression and alternative splicing in purified platelets from 120 peripheral blood samples constituting two independently collected and mutually validating patient cohorts of the three MPN subtypes: essential thrombocythemia, ET (n=24), polycythemia vera, PV (n=33), and primary or post ET/PV secondary myelofibrosis, MF (n=42), as well as healthy donors (n=21). The MPN platelet transcriptome discriminates each clinical phenotype and reveals an incremental molecular reprogramming that is independent of patient driver mutation status or therapy. Leveraging this dataset, in particular the progressive expression gradient noted across MPN, we develop a machine learning model (Lasso-penalized regression) predictive of the advanced subtype MF at high accuracy (AUC-ROC of 0.95-0.96) with validation under two conditions: i) temporal, with training on the first cohort (n=71) and independent testing on the second (n=49) and ii) 10 fold cross validation on the entire dataset. Lasso-derived signatures offer a robust core set of < 10 MPN progression markers. Mechanistic insights from our data highlight impaired protein homeostasis as a prominent driver of MPN evolution, with persistent integrated stress response. We also identify JAK inhibitor-specific signatures and other interferon, proliferation, and proteostasis associated markers as putative targets for MPN-directed therapy. Our platelet transcriptome snapshot of chronic MPNs establishes a methodological foundation for deciphering disease risk stratification and progression beyond genetic data alone, thus presenting a promising avenue toward potential utility in a wide range of age-related disorders.

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Keeping in touch with the membrane; protein- and lipid-mediated confinement of caveolae to the cell surface

Cited by 40 publications

References 71 publications

Caveolin-1 function at the plasma membrane and in intracellular compartments in cancer

Caveolin-1 function at the plasma membrane and in intracellular compartments in cancer

Lentinan Attenuated the PM2.5 Exposure-Induced Inflammatory Response, Epithelial–Mesenchymal Transition and Migration by Inhibiting the PVT1/miR-199a-5p/caveolin1 Pathway in Lung Cancer

Platelet transcriptome yields progressive markers in chronic myeloproliferative neoplasms and identifies putative targets of therapy

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