Journal Article10.1111/J.1755-148X.2011.00849.X
Melanoma cell invasiveness is regulated by miR-211 suppression of the BRN2 transcription factor
Glen M. Boyle,Susan L. Woods,Vanessa F. Bonazzi,Mitchell S. Stark,Elke Hacker,Elke Hacker,Lauren G. Aoude,Ken Dutton-Regester,Anthony L. Cook,Richard A. Sturm,Nicholas K. Hayward +10 more
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TL;DR: In this article, the most differentially expressed microRNA between the normal and tumor cell lines was miR-211, which is derived from the microphthalmia-associated transcription factor (MITF)-regulated gene, TRPM1 (melastatin).
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Abstract: To identify microRNAs potentially involved in melanomagenesis, we compared microRNA expression profiles between melanoma cell lines and cultured melanocytes. The most differentially expressed microRNA between the normal and tumor cell lines was miR-211. We focused on this pigment-cell-enriched miRNA as it is derived from the microphthalmia-associated transcription factor (MITF)-regulated gene, TRPM1 (melastatin). We find that miR-211 expression is greatly decreased in melanoma cells and melanoblasts compared to melanocytes. Bioinformatic analysis identified a large number of potential targets of miR-211, including POU3F2 (BRN2). Inhibition of miR-211 in normal melanocytes resulted in increased BRN2 protein, indicating that endogenous miR-211 represses BRN2 in differentiated cells. Over-expression of miR-211 in melanoma cell lines changed the invasive potential of the cells in vitro through directly targeting BRN2 translation. We propose a model for the apparent non-overlapping expression levels of BRN2 and MITF in melanoma, mediated by miR-211 expression.
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Citations
A novel recurrent mutation in MITF predisposes to familial and sporadic melanoma
Satoru Yokoyama,Susan L. Woods,Glen M. Boyle,Lauren G. Aoude,Stuart MacGregor,Victoria Zismann,Michael Gartside,Anne E. Cust,Rizwan Haq,Mark Harland,John C. Taylor,David L. Duffy,Kelly Holohan,Ken Dutton-Regester,Jane M. Palmer,Vanessa F. Bonazzi,Mitchell S. Stark,Judith Symmons,Matthew Law,Christopher W. Schmidt,Cathy Lanagan,Linda O'Connor,Elizabeth A. Holland,Helen Schmid,Judith A. Maskiell,Jodie Jetann,Megan Ferguson,Mark A. Jenkins,Richard F. Kefford,Graham G. Giles,Bruce K. Armstrong,Joanne F. Aitken,John L. Hopper,David C. Whiteman,Paul D.P. Pharoah,Douglas F. Easton,Alison M. Dunning,Julia Newton-Bishop,Grant W. Montgomery,Nicholas G. Martin,Graham J. Mann,D. Timothy Bishop,Hensin Tsao,Jeffrey M. Trent,David E. Fisher,Nicholas K. Hayward,Kevin M. Brown,Kevin M. Brown +47 more
TL;DR: Functional analysis of E318K showed that MITF encoded by the variant allele had impaired sumoylation and differentially regulated several MITF targets, indicating thatMITF is a melanoma-predisposition gene and highlight the utility of whole-genome sequencing to identify novel rare variants associated with disease susceptibility.
LncRNA loc285194 is a p53-regulated tumor suppressor
Qian Liu,Jianguo Huang,Nanjiang Zhou,Ziqiang Zhang,Ali Zhang,Zhaohui Lu,Fangting Wu,Yin-Yuan Mo +7 more
TL;DR: It is suggested that loc285194 is a p53-regulated tumor suppressor, which acts in part through repression of miR-211, and downregulation of loc285 194 in colon cancer specimens is detected.
The Master Neural Transcription Factor BRN2 Is an Androgen Receptor-Suppressed Driver of Neuroendocrine Differentiation in Prostate Cancer.
Jennifer L. Bishop,Daksh Thaper,Daksh Thaper,Sepideh Vahid,Sepideh Vahid,Alastair H. Davies,Kirsi Ketola,Hidetoshi Kuruma,Randy Jama,Ka Mun Nip,Ka Mun Nip,Arkhjamil Angeles,Fraser Johnson,Alexander W. Wyatt,Alexander W. Wyatt,Ladan Fazli,Ladan Fazli,Martin E. Gleave,Martin E. Gleave,Dong Lin,Mark A. Rubin,Colin Collins,Colin Collins,Yuzhuo Wang,Yuzhuo Wang,Himisha Beltran,Amina Zoubeidi,Amina Zoubeidi +27 more
TL;DR: First-in-field data underscore the consequences of potent AR inhibition in prostate tumors, revealing a novel mechanism of AR-dependent control of neuroendocrine differentiation, and uncover BRN2 as a potential therapeutic target to prevent emergence of NEPC.
MITF—the first 25 years
Colin R. Goding,Heinz Arnheiter +1 more
TL;DR: The current understanding of MITF's role and regulation in development and disease, as well as those of the MITF-related factors TFEB and TFE3, are presented, and key areas where the knowledge ofMITF regulation and function is limited are highlighted.
MITF in melanoma: mechanisms behind its expression and activity
TL;DR: The complexity of a multilevel regulation of MITF expression and activity that underlies distinct context-related phenotypes of melanoma and might explain diverse responses of melanomas patients to currently used therapeutics is discussed.
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