Identification of 14-3-3β Gene as a Novel miR-152 Target Using a Proteome-based Approach

Jasinski‐Bergner, Simon; Stehle, Franziska; Gonschorek, Evamaria; Kalich, J; Schulz, Kristin; Huettelmaier, Stefan; Braun, Juliane; Seliger, Barbara

doi:10.1074/jbc.m114.556290

Cited by 22 publications

(15 citation statements)

References 54 publications

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“…Whereas differentially expressed proteins were classified by a fold change ratio of 1.5 (increased or decreased) and a p-value of < 0.05, mass spectrometry analyses were performed on an ultrafleXtreme™ matrix-assisted laser desorption/ionization time of flight mass (MALDI-TOF) mass spectrometer (Bruker Daltonics Inc., Bremen, Germany). The resulting peptide mass fingerprinting datasets were analyzed using the MASCOT software package (Matrix Science, Dauheim, USA) [ 53 ].…”

Section: Methodsmentioning

confidence: 99%

Loss of epithelium-specific GPx2 results in aberrant cell fate decisions during intestinal differentiation

et al. 2017

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The selenoprotein glutathione peroxidase 2 (GPx2) is expressed in the epithelium of the gastrointestinal tract, where it is thought to be involved in maintaining mucosal homeostasis. To gain novel insights into the role of GPx2, proteomic profiles of colonic tissues either derived from wild type (WT) or GPx2 knockout (KO) mice, maintained under selenium (Se) deficiency or adequate Se supplementation conditions were established and analyzed. Amongst the panel of differentially expressed proteins, the calcium-activated chloride channel regulator 1 (CLCA1) was significantly down-regulated in GPx2 KO versus WT mice regardless of the given Se status. Moreover, transcript levels of the isoforms CLCA2 and CLCA3 showed a similar expression pattern. In the intestine, CLCA1 is usually restricted to mucin-producing goblet cells. However, although -SeKO mice had the highest numbers of goblet cells as confirmed by significantly enhanced mRNA expression levels of the goblet cell marker mucin-2, the observed expression pattern suggests that GPx2 KO goblet cells might be limited in synthesizing CLCA1. Furthermore, transcript levels of differentiation markers such as chromogranin-1 (Chga) for enteroendocrine cells and leucine-rich repeat-containing G-protein coupled receptor 5 (Lgr5) for stem cells were also downregulated in GPx2 KO mice. Moreover, this was accompanied by a downregulation of the mRNA expression levels of the intestinal hormones glucagon-like peptide 1 (Glp1), ghrelin (Ghrl) and somatostatin (Sst). Thus, it seems that GPx2 might be important for the modulation of cell fate decisions in the murine intestinal epithelium.

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Section: Methodsmentioning

confidence: 99%

Loss of epithelium-specific GPx2 results in aberrant cell fate decisions during intestinal differentiation

et al. 2017

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“…In cancer cells, the increased HLA-G expression is closely correlated with the loss of some HLA-Gtargeting miRNAs. Specifically, several members of miR-148 family such as miR-148a, miR-148b, and miR-152 could downregulate HLA-G expression [65][66][67]. In breast cancer cells, it was observed that oncogenic estrogenic G-protein-coupled estrogen receptor-1 (GPER) signaling pathway decreased downstream miR-148a level, further contributing to cancer immune evasion [68].…”

Section: Hla-g-targeting Mirnasmentioning

confidence: 99%

The role of cancer-derived microRNAs in cancer immune escape

et al. 2020

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During malignant transformation, accumulated somatic mutations endow cancer cells with increased invasiveness and immunogenicity. Under selective pressure, these highly immunogenic cancer cells develop multiple strategies to evade immune attack. It has been well established that cancer cells could downregulate the expression of major histocompatibility complex, acquire alterations in interferon pathway, and upregulate the activities of immune checkpoint pathways. Besides, cancer cells secret numerous cytokines, exosomes, and microvesicles to regulate the functions and abundances of components in the tumor microenvironment including immune effector cells and professional antigen presentation cells. As the vital determinant of post-transcriptional regulation, microRNAs (miRNAs) not only participate in cancer initiation and progression but also regulate anti-cancer immune response. For instance, some miRNAs affect cancer immune surveillance and immune escape by interfering the expression of immune attack-associated molecules. A growing body of evidence indicated that cancer-derived immune modulatory miRNAs might be promising targets to counteract cancer immune escape. In this review, we summarized the role of some miRNAs in cancer immune escape and discussed their potential clinical application as treatment targets.

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“…55 NIH/3T3 cells were stably transfected with the miR and/or the HLA-G expression vectors using the Effectene Transfection Reagent (Qiagen, Cat. no.…”

Section: Generation Of Hla-g and Mir Expression Vectors And Cell Tranmentioning

confidence: 99%

Clinical relevance of miR-mediated HLA-G regulation and the associated immune cell infiltration in renal cell carcinoma

et al. 2015

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In human tumors of distinct origin including renal cell carcinoma (RCC), the non-classical human leukocyte antigen G (HLA-G) is frequently expressed, thereby inhibiting the cytotoxic activity of T and natural killer (NK) cells. Recent studies demonstrated a strong post-transcriptional gene regulation of the HLA-G by miR-152, -148A, -148B and -133A. Standard methods were applied to characterize the expression and function of HLA-G, HLA-G-regulatory microRNAs (miRs) and the immune cell infiltration in 453 RCC lesions using a tissue microarray and five RCC cell lines linking these results to clinical parameters. Direct interactions with HLA-G regulatory miRs and the HLA-G 3' untranslated region (UTR) were detected and the affinities of these different miRs to the HLA-G 3'-UTR compared. qPCR analyses and immunohistochemical staining revealed an inverse expression of miR-148A and -133A with the HLA-G protein and. Stable miR overexpression caused a downregulation of HLA-G protein enhancing the NK and LAK cell-mediated cytotoxicity in CD107a activation assays revealing a HLA-G-dependent cytotoxic activity of immune effector cells. A significant higher frequency of CD3/CD8 T cell lymphocytes, but no differences in the activation markers CD69, CD25 or in the presence of CD56, FoxP3 and CD4 immune cells were detected in HLA-G compared to HLA-G RCC lesions. This could be associated with higher WHO grade, but not with a disease-specific survival. These data suggest a miR-mediated control of HLA-G expression in RCC, which is associated with a distinct pattern of immune cell infiltration.

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Identification of 14-3-3β Gene as a Novel miR-152 Target Using a Proteome-based Approach

Cited by 22 publications

References 54 publications

Loss of epithelium-specific GPx2 results in aberrant cell fate decisions during intestinal differentiation

Loss of epithelium-specific GPx2 results in aberrant cell fate decisions during intestinal differentiation

The role of cancer-derived microRNAs in cancer immune escape

Clinical relevance of miR-mediated HLA-G regulation and the associated immune cell infiltration in renal cell carcinoma

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