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Expression data from WT and Cavin-3 knockout mice adipose tissue

ABSTRACT: The cavins are a family of proteins associated with caveolae, cavin-1, -2 and -3 being widely expressed while cavin-4 is restricted to striated muscle. Deletion of cavin-1 results in phenotypes including metabolic changes consistent with adipocyte dysfunction, and caveolae are completely absent. Deletion of cavin-2 causes tissue-specific loss of caveolae. The consequences of cavin-3 deletion are less clear, as there are divergent data on the abundance of caveolae in cavin-3 null mice. Here we examine the consequences of cavin-3 deficiency in vivo by making cavin-3 knockout mice. Microarray analysis from adipose tissue shows that the changes in mRNA expression between cavin-3 null and wild type mouse are minimal.

ORGANISM(S): Mus musculus

PROVIDER: GSE57513 | GEO | 2016/12/31

SECONDARY ACCESSION(S): PRJNA246576

REPOSITORIES: GEO

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Cavin-3 Dictates the Balance Between ERK and Akt Signaling

Project description:Cavin-3 is a tumor suppressor protein of unknown function. Using a combination of in vivo knockout and in vitro gain/loss of function approaches, we show that cavin-3 dictates the balance between ERK and Akt signaling. Loss of cavin-3 increases Akt signaling at the expense of ERK, while gain of cavin-3 increases ERK signaling at the expense Akt. Cavin-3 facilitates signal transduction to ERK by anchoring caveolae, a lipid-raft specialization that contains an ERK activation module, to the membrane skeleton of the plasma membrane. Loss of cavin-3 reduces the number of caveolae, thereby separating this ERK activation module from signaling receptors. Loss of cavin-3 promotes Akt signaling through suppression of EGR1 and PTEN. The in vitro consequences of the loss of cavin-3 include induction of Warburg metabolism (aerobic glycolysis), accelerated cell proliferation and resistance to apoptosis. The in vivo consequences of cavin-3 loss are increased lactate production and cachexia. 9 total samples, consisting of 3 cavin-3 siRNA groups (0 days, 3 days and 8 days) one set was untreated, one set was serum starved, one set was serum starved and then treated with EGF for 1 hr.

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Project description:This study assessed exosomal and cellular miRNA profiles in GFP-PC3 cells and ectopically expressed cavin-1 PC3 cell lines. To understand the consequences of cavin-1 on extracellular vesicle (EV)-contained miRNAs, a small RNA-seq experiment was performed on cells and secreted EVs for GFP-PC3 and cavin-1-PC3 cells. Small RNA were selected for sequencing using the NEBNext Small RNA library Prep Kit. Libraries were size selected using a Perkin Elmer Labchip XT. Whole cell and EV libraries were multiplexed from three biological replicates and sequenced on an Illumina NextSeq500 mid-output run at a read depth of 1million reads per sample. While the raw data was mapped to the human miRNAome using RNA-STAR and miRBase (v21) as reference, 317 mature miRNAs were identified in EVs at varying abundances depending on cell of origin. The 317 miRNAs identified in both cell and EVs were further processed. After RUVseq normalization, DESeq2 analysis was used to identify differences between cellular miRNA profiles and EV miRNA profiles from the two different cell lines. This analysis ultimately defined the repertoire of selectively and passively exported exosomal miRNAs mediated by non-caveolar caveolin-1 and cavin-1 in a prostate cancer cell line. Aim: To assess exosomal miRNA compositional changes evoked by ectopic expression of cavin-1 in the PC3 advanced prostate cancer cell line. Objectives: 1. Determine differential expression of miRNAs in cells and 2. determine differential abundance of miRNAs in extracellular vesicles secreted from cavin-1 expressing or GFP expressing cells.

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