Lymphoproliferative disease and autoimmunity in mice with increased miR-17-92 expression in lymphocytes

By Changchun Xiao, L. Srinivasan, D. Calado, H. C. Patterson, Baochun Zhang, Jing Wang, J. Henderson, J. Kutok, K. Rajewsky. Nature Immunology, 2008

1,297 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/a28ed21eba3b934f5c285379ed74f57ae9274b8a

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Citations in the corpus

Role of microRNAs in vascular diseases, inflammation, and angiogenesis. (2008, background): “Overexpression of the miR-17-92 cluster in lymphocytes additionally induces lymphoproliferative disease and autoimmunity.(74) MiRNAs also modulate monocyte differentiation and function.”
MicroRNAs in cancer: small molecules with a huge impact. (2009, background): “More recently, a different group observed that the overexpression of miR-17-92 in lymphocytes caused a lymphoproliferative disease, autoimmunity, and premature death.(13) The enhanced proliferation of the transgenic lymphocytes was mediated by direct regulation of pro-apoptotic phosphatase and tensi”
The miR-17/92 cluster: a comprehensive update on its genomics, genetics, functions and increasingly important and numerous roles in health and disease (2013, neutral): “On the other hand, overexpression of the cluster was also shown to cause lymphoproliferative diseases.(44) Parallel studies have also implicated miR-17/92 in normal lymphocyte development.”
MicroRNAs in human cancer. (2013, background): “disorder, and higher level expression of the cluster in MYC-driven B-cell lymphomas dramatically increased tumorigenicity [ 62, 173 ] .”
Causes and consequences of microRNA dysregulation in cancer (2009, background): “Recent studies of gain and loss of function indicated that this cluster is essential for B cell proliferation and that overexpression in B cells induces a lymphoproliferative disorder in mic”
MicroRNAs en route to the clinic: progress in validating and targeting microRNAs for cancer therapy (2011, neutral): “The mir-17∼92 cluster and its paralogues, mir-106b∼25 and mir-106a∼363 , are several such regions that have been extensively examine”
Inositol phosphatase SHIP1 is a primary target of miR-155 (2009, background): “Similar observations have been made for specific targets of miR-150 (11, 50), miR-223 (6), and miR-17–92 (10, 12), suggesting a common theme of a few significant targets making dominant contributions to miRNA function.”
MicroRNAs and cancer: short RNAs go a long way. (2009, background): “…miR-17~92 deregulation does not appear to be sufficient to initiate tumorigenesis per se, transgenic mice overexpressing this cluster in lymphocyte progenitor cells develop a lymphoproliferative disorder affecting both B and T cells that eventually results in autoimmunity (Xiao et al., 2008).”
microRNA regulation of inflammatory responses. (2012, background): “In T cells, miRNAs in the miR-17 to miR-92 cluster are involved in managing cell survival by repressing BIM and PTEN, both of which potentiate cell death (48).”
Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs (2011, neutral): “…Berger et al., 2011; Trotman et al., 2003), and (3) numerous microRNAs have beenvalidatedasPTENregulators, including theproto-oncogenic miR-106b 25 cluster that is overexpressed in prostate cancer (Huse et al., 2009; Mu et al., 2009; Olive et al., 2009; Poliseno et al., 2010a; Xiao et al., 2008).”
MicroRNA-155 promotes autoimmune inflammation by enhancing inflammatory T cell development (2010, background): “For instance, enforced expression of the miR-17-92 cluster in T cells or specific deletion of Dicer in T regulatory (Treg) cells both trigger lethal autoimmune conditions (Chong et al., 2008; Liston et al., 2008; Xiao et al., 2008; Zhou et al., 2008).”
PDL1 Regulation by p53 via miR-34 (2015, background): “For instance, several p53-regulated miRNAs have been implicated in adaptive and innate immunity, including the miR-17~92 cluster (11), miR-145 (12), and let-7 (13).”
The transcriptional repressor Bcl-6 directs T follicular helper cell lineage commitment. (2009, background): “It is interesting to note that mice transgenic for miR-17-92 display abnormal compartmentalization and segregation of B cells and T cells in secondary lymphoid organs and paucity of B cells within follicular structures (Xiao et al., 2008).”