miR-15 and miR-16 induce apoptosis by targeting BCL2.

By A. Cimmino, George A. Calin, M. Fabbri, Marilena V. Iorio, M. Ferracin, M. Shimizu, Sylwia E. Wojcik, R. Aqeilan, S. Zupo, M. Dono and 7 more. Proceedings of the National Academy of Sciences of the United States of America, 2005

3,834 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/b7934a805a4da4737ef73943fcc96ccbb5ed8379

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Citations in the corpus

MiR-221 controls CDKN1C/p57 and CDKN1B/p27 expression in human hepatocellular carcinoma (2008, background): “Nevertheless, in spite of the discovery of various miRNA targets implicated in human cancer (Cimmino et al., 2005; Johnson et al., 2005; O’Donnell et al., 2005), most mechanisms by which miRNAs are involved in tumorigenesis remain to be elucidated.”
Cyclin G1 is a target of miR-122a, a microRNA frequently down-regulated in human hepatocellular carcinoma. (2007, background): “Only few studies have identified oncogenes whose level of expression is regulated by miRNAs: members of the let-7 miRNA family can regulate all three members of the RAS oncogene family (30) and mir-15a/mir-16-1 regulate BCL2 (39).”
The miR-15a–miR-16-1 cluster controls prostate cancer by targeting multiple oncogenic activities (2008, background): “These observations suggest the existence of tumor suppressor gene(s) involved in prostate carcinogenesis within the 13q14 regio”
Epigenetic silencing of microRNA-34b/c and B-cell translocation gene 4 is associated with CpG island methylation in colorectal cancer. (2008, background): “thought to target the antiapoptotic factor BCL2, is frequently diminished (8).”
MicroRNA-34b and MicroRNA-34c are targets of p53 and cooperate in control of cell proliferation and adhesion-independent growth. (2007, background): “For example, miR-15a and miR-16 target antiapoptotic gene BCL-2 (2), whereas the LATS32 tumor suppressor is targeted by miR-372 and miR-373 (3).”
Apoptosis and cancer: the genesis of a research field (2009, background): “Since these discoveries, several other mechanisms have been identified that can lead to increased BCL-2 expression, including hypermethylation of BCL2 and loss of microRNAs that normally downregulate BCL-2 expressio”
Transcripts Targeted by the MicroRNA-16 Family Cooperatively Regulate Cell Cycle Progression (2007, background): “Cimmino et al. showed that miR-15 and miR-16 negatively regulate the antiapoptotic protein BCL2 (14).”
The DLEU2/miR-15a/16-1 cluster controls B cell proliferation and its deletion leads to chronic lymphocytic leukemia. (2010, background): “Although DLEU2 and the miRs are evolutionary conserved and expressed in B cells (Cimmino et al., 2005; Mertens et al., 2002; Migliazza et al., 2001), a role of DLEU1 as well as the adjacent DLEU5 and KCNRG genes (Ivanov et al.”
Specific activation of microRNA-127 with downregulation of the proto-oncogene BCL6 by chromatin-modifying drugs in human cancer cells. (2006, background): “10 oncogene, RAS, and miR-15 and 16, which are downregulated in chronic lymphocytic leukemias, target an antiapoptotic factor, BCL2 (Cimmino et al., 2005; Johnson et al., 2005).”
Identification of metastasis‐related microRNAs in hepatocellular carcinoma (2008, neutral): “0001 TNM Stage I 99 (41) 66 (50) 33 (30) II 87 (36) 34 (26) 53 (48) III 55 (23) 31 (24) 24 (22) 0.”
microRNAs as oncogenes and tumor suppressors. (2007, background): “For example, miR-15 and miR-16 induce apoptosis by targeting antiapoptotic gene B cell lymphoma 2 (BCL2) mRNA (Cimmino et al., 2005), which is a key player in many types of human cancers, including leukemias, lymphomas, and carcinomas (Sanchez-Beato et al., 2003).”
Epigenetic gene silencing in cancer: the DNA hypermethylome. (2007, background): “For example, the downregulated let-7 and miR-15/miR-16, and miR-127 are known to target the oncogenic factors RAS and BCL-2, respectively (97,98).”