The secretory small GTPase Rab27B as a marker for breast cancer progression

Hendrix, An; Braems, Geert; Bracke, Marc; Seabra, Miguel C.; Gahl, William A.; Wever, Olivier De; Westbroek, Wendy

doi:10.18632/oncotarget.140

Cited by 36 publications

(12 citation statements)

References 21 publications

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“…Equivalent amounts of total protein, as determined by BCA assay (Pierce Biotechnology, Rockford, IL, USA), from HEK cells or control and patient melanocyte extracts, were loaded onto 4–12% Tris‐Glycine gels. After blotting, the nitrocellulose membranes (Invitrogen) were probed with a rabbit polyclonal antibody specific for RAB27B (Barral et al., 2002), a mouse monoclonal antibody specific for RAB27A [BD Biosciences, San Jose, CA, USA; (Hendrix et al., 2010a)], a mouse monoclonal α‐tubulin antibody (loading control, Sigma), a GFP mouse monoclonal antibody (Millipore), a mouse monoclonal MYO5A antibody (Sigma), and a rabbit polyclonal MLPH antibody (Proteintech Group Inc.), followed by incubation with HRP‐labeled secondary anti‐mouse or anti‐rabbit antibodies (Amersham Biosciences, Piscataway, NJ, USA). The antigen–antibody complexes were detected with an Enhanced Chemiluminescence (ECL) kit (Amersham Biosciences).…”

Section: Methodsmentioning

confidence: 99%

Cellular and clinical report of new Griscelli syndrome type III cases

Westbroek

Klar

Cullinane

et al. 2011

Pigment Cell Melanoma Res

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Summary The RAB27A/Melanophilin/Myosin-5a tripartite protein complex is required for capturing mature melanosomes in the peripheral actin network of melanocytes for subsequent transfer to keratinocytes. Mutations in any one member of this tripartite complex cause three forms of Griscelli syndrome (GS), each with distinct clinical features but with a similar cellular phenotype. To date, only one case of GS type III (GSIII), caused by mutations in the Melanophilin (MLPH) gene, has been reported. Here we report seven new cases of GSIII in three distinct Arab pedigrees. All affected individuals carried a homozygous missense mutation (c.102C>T; p.R35W), located in the conserved Slp homology domain (SHD) of MLPH, and had hypomelanosis of the skin and hair. We report the first cellular studies on GSIII melanocytes, which demonstrated that MLPH(R35W) causes perinuclear aggregation of melanosomes in melanocytes, typical for GS. Additionally, co-immunoprecipitation assays showed that MLPH(R35W) lost its interaction with RAB27A, indicating pathogenicity of the R35W mutation.

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Section: Methodsmentioning

confidence: 99%

Cellular and clinical report of new Griscelli syndrome type III cases

Westbroek

Klar

Cullinane

et al. 2011

Pigment Cell Melanoma Res

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“…Because exosome secretion is closely related to cancer and tumor progression (124), increased Rab27dependent exosome secretion may cause cancer or tumors. It is particularly noteworthy that alteration of Rab27 expression has often been observed in cancer cells (125)(126)(127)(128) and that overexpression and knockdown of Rab27 in cancer cells have been found to affect their invasiveness (129)(130)(131)(132).…”

Section: Role Of Rab27 Effectors In the Secretory Pathways Of Secretomentioning

confidence: 99%

Rab27 Effectors, Pleiotropic Regulators in Secretory Pathways

Fukuda¹

2013

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Rab27, a member of the small GTPase Rab family, is widely conserved in metazoan, and two Rab27 isoforms, Rab27A and Rab27B, are present in vertebrates. Rab27A was the first Rab protein whose dysfunction was found to cause a human hereditary disease, type 2 Griscelli syndrome, which is characterized by silvery hair and immunodeficiency. The discovery in the 21st century of three distinct types of mammalian Rab27A effectors [synaptotagmin-like protein (Slp), Slp homologue lacking C2 domains (Slac2), and Munc13-4] that specifically bind active Rab27A has greatly accelerated our understanding not only of the molecular mechanisms of Rab27A-mediated membrane traffic (e.g. melanosome transport and regulated secretion) but of the symptoms of Griscelli syndrome patients at the molecular level. Because Rab27B is widely expressed in various tissues together with Rab27A and has been found to have the ability to bind all of the Rab27A effectors that have been tested, Rab27A and Rab27B were initially thought to function redundantly by sharing common Rab27 effectors. However, recent evidence has indicated that by interacting with different Rab27 effectors Rab27A and Rab27B play different roles in special types of secretion (e.g. exosome secretion and mast cell secretion) even within the same cell type. In this review article, I describe the current state of our understanding of the functions of Rab27 effectors in secretory pathways.

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“…reprogramming from oxidative phosphorylation towards aerobic glycolysis in breast cancer cells [11]. Clinical studies indicated that the elevated expression of Rab27b was correlated with lymph node metastasis and the secretory Rab27b was an independent risk factor for survival of breast cancer patients [12]. [14].…”

Section: Overexpression Of Rab27b Enhanced the Invasive Capacities Anmentioning

confidence: 99%

Exosomes: Potent regulators of tumor malignancy and potential bio-tools in clinical application

Guo¹,

Guo²

2015

Critical Reviews in Oncology/Hematology

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Multiple lines of evidence indicate that exosomes, as efficient messengers in cell-to-cell communication, play pleiotropic roles in regulating tumor malignancy. The cargos (proteins, mRNAs, and miRNAs) carried by exosomes can be functionally delivered between different types of cells and even transferred to distant locations, influencing the biological activities of tumor and non-tumor cells and promoting tumor growth, invasion, metastasis, angiogenesis, and drug resistance. Tumor-associated exosomes have been identified in biological (plasma, urine, saliva) and pathological (malignant effusions, pleural effusions, ascites) fluids from cancer patients. The contents of exosomes may vary depending on tumor types and status. Detection of exosomes in biofluids of cancer patients may represent a promising strategy to gain pathogenic information and to select specific biomarkers for the diagnosis and prognosis of cancer. Utilization of exosomes as delivery vehicles for siRNAs and therapeutic drugs brings out new concepts such as biomimetics in cancer treatment. In this review, we will mainly discuss emerging roles of exosomes in tumor invasion, metastasis, angiogenesis, and drug resistance and potential clinical application of exosomes as biomarkers and therapeutic tools.

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The secretory small GTPase Rab27B as a marker for breast cancer progression

Cited by 36 publications

References 21 publications

Cellular and clinical report of new Griscelli syndrome type III cases

Cellular and clinical report of new Griscelli syndrome type III cases

Rab27 Effectors, Pleiotropic Regulators in Secretory Pathways

Exosomes: Potent regulators of tumor malignancy and potential bio-tools in clinical application

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