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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | McGirt, Laura Y. Adams, Clare M. Baerenwald, Devin A. Zwerner, Jeffrey P. Zic, John A. Eischen, Christine M. |
| Description | Country affiliation: United States Author Affiliation: McGirt LY ( Department of Medicine/Dermatology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.); Adams CM ( Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.); Baerenwald DA ( Department of Medicine/Dermatology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.); Zwerner JP ( Department of Medicine/Dermatology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.); Zic JA ( Department of Medicine/Dermatology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.); Eischen CM ( Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.) |
| Abstract | The pathogenesis of the cutaneous T-cell lymphoma (CTCL), mycosis fungoides (MF), is unclear. MicroRNA (miRNA) are small noncoding RNAs that target mRNA leading to reduced mRNA translation. Recently, specific miRNA were shown to be altered in CTCL. We detected significantly reduced expression of miR-223 in early-stage MF skin, and further decreased levels of miR-223 in advanced-stage disease. CTCL peripheral blood mononuclear cells and cell lines also had reduced miR-223 as compared with controls. Elevated expression of miR-223 in these cell lines reduced cell growth and clonogenic potential, whereas inhibition of miR-223 increased cell numbers. Investigations into putative miR-223 targets with oncogenic function, including E2F1 and MEF2C, and the predicted miR-223 target, TOX, revealed that all three were targeted by miR-223 in CTCL. E2F1, MEF2C, and TOX proteins were decreased with miR-223 overexpression, whereas miR-223 inhibition led to increased protein levels in CTCL. In addition, we showed that the 3'-UTR of TOX mRNA was a genuine target of miR-223. Therefore, reduced levels of miR-223 in MF/CTCL lead to increased expression of E2F1, MEF2C, and TOX, which likely contributes to the development and/or progression of CTCL. Thus, miR-223 and its targets may be useful for the development of new therapeutics for MF/CTCL. |
| File Format | HTM / HTML |
| ISSN | 0022202X |
| e-ISSN | 15231747 |
| DOI | 10.1038/jid.2013.461 |
| Journal | Journal of Investigative Dermatology |
| Issue Number | 4 |
| Volume Number | 134 |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2014-04-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Discipline Dermatology Gene Expression Regulation, Neoplastic Lymphoma, T-cell, Cutaneous Genetics Metabolism Micrornas Mycosis Fungoides 3' Untranslated Regions Animals Biopsy Cell Line, Tumor Cell Proliferation Cell Survival Disease Progression Gene Expression Profiling Leukocytes, Mononuclear Cytology Mice Nih 3t3 Cells Proto-oncogenes Skin Pathology Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology Dermatology |
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