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Mining Meningioma Proteomics Alterations Using IP MS

ABSTRACT: Herein we have used IP-MS based approach to identify potential interactors (PPI) that bind to Annexin A2. We have used Immunoaffinity based enrichment using antibody specific to ANXA2 followed by LC MS-MS of the Complex post running it in SDS-PAGE

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Brain, Epithelial Cell

DISEASE(S): Brain Cancer

SUBMITTER: Shuvolina Mukherjee

LAB HEAD: SANJEEVA SRIVASTAVA

PROVIDER: PXD014853 | Pride | 2021-08-30

REPOSITORIES: Pride

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Comprehending Meningioma Signaling Cascades Using Multipronged Proteomics Approaches & Targeted Validation of Potential Markers.

Mukherjee Shuvolina S Biswas Deeptarup D Gadre Rucha R Jain Pooja P Syed Nelofer N Stylianou Julianna J Zeng Qingyu Q Mahadevan Anita A Epari Sridhar S Shetty Prakash P Moiyadi Aliasgar A Roy Ball Graham G Srivastava Sanjeeva S

Frontiers in oncology 20200826

Meningiomas are one of the most prevalent primary brain tumors. Our study aims to obtain mechanistic insights of meningioma pathobiology using mass spectrometry-based label-free quantitative proteome analysis to identifying druggable targets and perturbed pathways for therapeutic intervention. Label-free based proteomics study was done from peptide samples of 21 patients and 8 non-tumor controls which were followed up with Phosphoproteomics to identify the kinases and phosphorylated components o ...[more]

PMID: 32974197

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Role of annexin A2 in muscle repair

Project description:Repair of injured muscle involves repair of injured myofibers through the involvement of dysferlin and its interacting partners, including annexin. Studies with mice and patients have established that dysferlin deficit leads to chronic inflammation and adipogenic replacement of the diseased muscle. However, longitudinal analysis of annexin deficit on muscle pathology and function is lacking. Here we show that unlike annexin A1, but similar to dysferlin, lack of annexin A2 (AnxA2) causes poor myofiber repair and progressive weakening with age. However, unlike dysferlin-deficient muscle, AnxA2-deficient muscles do not exhibit chronic inflammation or adipogenic replacement. Deletion of AnxA2 in dysferlin deficient mice reduces inflammation, adipogenic replacement, and loss in muscle function caused by dysferlin deficit. These results show that: a) AnxA2 facilitates myofiber repair, b) chronic inflammation and adipogenic replacement of dysferlinopathic muscle requires AnxA2, and c) inhibiting AnxA2-mediated inflammation is a novel therapeutic avenue for dysferlinopathy.

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Annexin A2 Modulates Radiation-Sensitive Transcriptional Programming and Cell Fate

Project description:Whole genome expression profiling in the presence and absence of annexin A2 [shRNA] identified fundamentally altered transcriptional programming that changes the radioresponsive transcriptome. Bioinformatics predicted that silencing AnxA2 may enhance cell death responses to stress in association with reduced activation of pro-survival signals such as nuclear factor kappa B. This prediction was validated by demonstrating a significant increase in sensitivity toward tumor necrosis factor alpha induced cell death in annexin A2 silenced cells, relative to vector controls, associated with reduced nuclear translocation of RelA (p65) following tumor necrosis factor alpha treatment. Murine progenitor cells, JB6 cell line, were stably transformed with Annexin A2 shRNA or vector only control and then treated with ionizing radiation at two doses, 10cGy and 100cGy. Samples were collected at 2hr, 6hr and 24hr for RNA isolation. Two untreated time points were collected also: 2hr and 24hr.

2012-11-28 | E-GEOD-42547 | biostudies-arrayexpress

Annexin A2 Modulates Radiation-Sensitive Transcriptional Programming and Cell Fate

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RNA-seq analysis of transcriptomes in Wild Type and ANXA2 knockdown HK2 cells

Project description:We conducted this experiment to study the effects of Annexin A2 (ANXA2) on gene expression in human proximal tubular epithelial (HK2) cells in vitro. Short hairpin RNA targeting ANXA2 was designed and cloned into vector pGFP-B-RS for RNAi to generate the recombinant expression plasmids, which were transfected into HK2 cells. RNA-seq analysis were performed on HK2 cells, with or without ANXA2 knockdown, to reveal the differentially expressed genes (DEGs) and regulated alternative splicing events (RASEs). Then the DEGs and RASEs were validated by qRT-PCR. Using criteria of an absolute fold change of ≥2.0 or ≤ 0.5 and false discovery rate (FDR) of < 0.05 with the edgeR package, RNA-seq analysis of the transcriptomes revealed 220 upregulated and 171 downregulated genes related to ANXA2 knockdown.

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Project description:We have previously established two sibling glioma subclones, J3T-1 and J3T-2, showing distinct invasive and angiogenic phenotypes. J3T-1, expressing high annexin A2, demonstrates robust angiogenesis and tumor invasion around neovasculature. J3T-2, expressing low annexin A2, demonstrates diffuse invasion along white matter tracts. Knockdown of annexin A2 in J3T-1 (J3T-1shA) resulted in diffuse invasion pattern, and overexpression of annexin A2 in J3T-2 (J3T-2A) showed prominent angiogenesis. We used microarrays to identify genes which promote the phenotypic transition regulated by annexin A2.

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Project description:We previously demonstrated that Annexin A2 (ANXA2) is a pivotal mediator of the pro-oncogenic features displayed by glioblastoma (GBM) tumors, the deadliest adult brain malignancies. In GBM, ANXA2 sustains a transcriptional program involved in cell stemness, proliferation and invasion, negatively impacting patient prognosis. Transcriptional signatures obtained by the modulation of ANXA2 activity/levels were functionally mapped through the QUADrATiC bioinformatic tool for compound identification. Selected compounds were screened by cell proliferation and migration assays in primary GBM cells. Screening of compounds selected through QUADrATiC identified HHT as a potent inhibitor of GBM cell motility and proliferation. A further molecular characterization of the effects displayed by HHT, confirmed its ability to inhibit a transcriptional program involved in cell migration and invasion. Moreover, we demonstrated that the multiple antitumoral effects displayed by HHT are correlated to the inhibition of a PDGFRα-dependent intracellular signaling through the impairment of STAT3 and RhoA axes. Homoharringtonine is a potent inhibitor of GBM cell proliferation and migration

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Activation of YAP-dependent Proliferation by a Small Molecule Targeting Annexin A2

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