The miR-15a–miR-16-1 cluster controls prostate cancer by targeting multiple oncogenic activities
By D. Bonci, V. Coppola, M. Musumeci, A. Addario, R. Giuffrida, L. Memeo, L. D’Urso, A. Pagliuca, M. Biffoni, C. Labbaye and 4 more. Nature Medicine, 2008
1,007 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/289b80ae2660e76442c6492b4549f400979e9bec
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cancer Research
- Phillip A. Sharp
- Margaret S. Ebert
- Carlo Maria Croce
- Danish H Sayed
- M. Abdellatif
- A. Ventura
- T. Jacks
- George A. Calin
In Molecular Biology
- Phillip A. Sharp
- Margaret S. Ebert
- Carlo Maria Croce
- M. Abdellatif
- Danish H Sayed
- C. Abate-Shen
- A. Ventura
- M. Shen
Citations in the corpus
- Diagnostic and prognostic implications of microRNA profiling in prostate carcinoma (2009, background): “Downregulation of miR-16 has also been observed in prostate cancer samples(13) and in primary cells received from patients with pT2 and pT3 tumors.(30) Reconstitution of hsamiR-16 levels in LNCaP cells and primary tumor cells led to growth arrest and apoptosis.”
- Causes and consequences of microRNA dysregulation in cancer (2009, background): “have shown that the miR-15a–miR-16-1 cluster can control prostate cancer by targeting multiple oncogenic activitie”
- From pathogenesis to treatment of chronic lymphocytic leukaemia (2010, background): “Deletions at 13q14 occur at high frequencies in other lymphomas and solid tumours, and a recent study has implicated miR-15a and miR-16-1 in the pathogenesis of prostate cancer through their targeting of cyclin D1 and WNT3A, which promote survival and proliferatio”
- Targeting MicroRNAs in Cancer: Rationale, Strategies and Challenges (2010, neutral): “In addition miR-15a–miR16-1 was found to be downregulated in CLL, prostate and pituitary adenoma”
- MicroRNA sponges: progress and possibilities. (2010, background): “Sponges with sites perfectly complementary to the miRNA show some inhibitory activity (Carè et al. 2007; Ebert et al. 2007; Scherr et al. 2007; Bonci et al. 2008; Sayed et al. 2008; Gentner et al. 2009; Haraguchi et al. 2009; Horie et al. 2009; Huang et al. 2010; Papapetrou et al. 2010), perhaps…”
- MicroRNAs in development and disease. (2011, background): “Reduced levels of miR-15/16 are associated with an increase in the protein levels of their targets Bcl2, cyclin D1, and WNT3A (53) that is known to enhance CaP growth and stem cell self-renewal (46, 363, 635).”
- Cyclin D as a therapeutic target in cancer (2011, background): “Their expression is inversely correlated with cyclin D1 expression in the small series of prostate and lung cancers that have been examined to dat”
- Molecular genetics of prostate cancer: new prospects for old challenges. (2010, background): “…expression of CCND1, WNT3A, and BCL2 in prostate cancer have provided an example of potential therapeutic benefit in restoring expression of miRNAs (Bonci et al. 2008), while detection of miRNAs in human plasma has been proposed as a platform for blood-based detection of human cancer (Mitchell et…”
- MicroRNAs and cancer: short RNAs go a long way. (2009, background): “Accordingly, a recent study has shown that inhibition of miR-15a and miR-16 activity leads to hyperplasia of the prostate in mice and promotes survival, proliferation, and invasion of primary prostate cells in vitro (Bonci et al., 2008).”