The Promyelocytic Leukemia Zinc Finger–MicroRNA-221/-222 Pathway Controls Melanoma Progression through Multiple Oncogenic Mechanisms

Felicetti, Federica; Errico, Maria Cristina; Bottero, Lisabianca; Segnalini, Patrizia; Stoppacciaro, Antonella; Biffoni, Mauro; Felli, Nadia; Mattia, Gianfranco; Petrini, Marina; Colombo, Mario P.; Peschle, Cesare; Caré, Alessandra

doi:10.1158/0008-5472.can-07-2538

Cited by 344 publications

(309 citation statements)

References 40 publications

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“…8,12,13,32 In this study, T-LBL/ALL patients with any bone marrow involvement showed shorter event-free survival, which was consistent with previous report. 33 Although PLZF was a strong indicator for initial bone marrow involvement of any quantity in this study, PLZF expression itself had no influence on the survival of T-LBL/ALL patients.…”

Section: Discussionsupporting

confidence: 92%

“…[7][8][9][10][11] PLZF also has a role in skeletal development and spermatogenesis, and it has a tumor-suppressive role in a few solid tumors. 1,[12][13][14][15] It was recently found that PLZF is essential for the development of natural killer T (NKT) cells and acquisition of the unique innate-like characteristics of innate T cells. [16][17][18][19] Innate immunity is mediated by natural killer (NK) cells, monocytes/macrophages, and granulocytes.…”

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confidence: 99%

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Expression of the promyelocytic leukemia zinc-finger in T-lymphoblastic lymphoma and leukemia has strong implications for their cellular origin and greater association with initial bone marrow involvement

Jeon

Nam

et al. 2012

Modern Pathology

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The promyelocytic leukemia zinc-finger (PLZF) is essential for the development of innate T cells (as represented by natural killer T cells) for acquisition of their unique innate immune properties. We evaluated the PLZF protein expression in a variety of immature and mature lymphoid malignancies. PLZF was preferentially expressed in T-lymphoblastic lymphoma/acute lymphoblastic leukemia (T-LBL/ALL) in 50% of the 54 cases. Among 51 cases of peripheral T-cell lymphoma not otherwise specified, only one (2%) expressed PLZF. One mycosis fungoides case expressed PLZF in lymph node involved by tumor. Otherwise, PLZF was not detected in any other type of lymphoma. In T-LBL/ALL, PLZF expression was more common in CD4/CD8 double-negative (67%) or CD8 single-positive subtypes (73%) than in CD4/CD8 double-positive (13%) and CD4 single-positive subtypes (0%) (P ¼ 0.001). Importantly, PLZF and CD1a expression were mutually exclusive in T-LBL/ALL (P ¼ 0.001). This was also the case for T-cell receptor bF1 expression (P ¼ 0.000). Most (96%) of the PLZF-positive T-LBL/ALL cases showed initial bone marrow involvement compared with 39% of PLZF-negative cases (P ¼ 0.000). Based on these findings, we suggest that T-LBL/ALLs that express PLZF arise from early immature double-negative thymocytes when the T-cell receptor b chain has not yet expressed or innate T-cell precursors, and strongly imply bone marrow involvement.

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Section: Discussionsupporting

confidence: 92%

mentioning

confidence: 99%

Expression of the promyelocytic leukemia zinc-finger in T-lymphoblastic lymphoma and leukemia has strong implications for their cellular origin and greater association with initial bone marrow involvement

Jeon

Nam

et al. 2012

Modern Pathology

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“…The first reports linking altered expression of a single miRNA to a function in melanoma tumorigenesis and conducting detailed comparisons of the miRNA profiles Novel oncogenic role for miRNA-506-514 cluster in melanoma KL Streicher et al of normal melanocytes and melanoma cell lines have only recently been published (Felicetti et al, 2008;. The ability of miR-221 and miR-222 to regulate the c-Kit receptor (Felicetti et al, 2008), miR-let-7b to inhibit cell-cycle progression (Schultz et al, 2008) and miR-193b to induce cell-cycle arrest by altering CCND1 (Chen et al, 2010) illustrate a few studies that contain functional experiments linking miRNA alterations to melanoma development/progression.…”

Section: Discussionmentioning

confidence: 99%

“…The ability of miR-221 and miR-222 to regulate the c-Kit receptor (Felicetti et al, 2008), miR-let-7b to inhibit cell-cycle progression (Schultz et al, 2008) and miR-193b to induce cell-cycle arrest by altering CCND1 (Chen et al, 2010) illustrate a few studies that contain functional experiments linking miRNA alterations to melanoma development/progression. However, the potential roles for miRNAs as diagnostic biomarkers or as targets have yet to be investigated fully in melanoma.…”

Section: Discussionmentioning

confidence: 99%

“…Significant data have accumulated showing that dysregulated miRNAs act as oncogenes (onco-miRs) or tumor suppressors (TS-miRs) through their effects on various pathways critical to the cancer phenotype (Landais et al, 2007;Sotiropoulou et al, 2009;Segura et al, 2010). Multiple studies have characterized these dysregulated miRNAs in diverse cancer types, including melanoma (Lu et al, 2005;Felicetti et al, 2008;Mirnezami et al, 2009;Sotiropoulou et al, 2009). Evidence also exists that miRNA clusters can have oncogenic properties in cancer, where the role of the miR-17-92 cluster in lymphoma has been the most extensively characterized (Olive et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

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A novel oncogenic role for the miRNA-506-514 cluster in initiating melanocyte transformation and promoting melanoma growth

et al. 2011

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Malignant melanoma is the most aggressive form of skin cancer and its incidence has doubled in the last two decades. It represents only 4% of skin cancer cases per year, but causes as many as 74% of skin cancer deaths. Early detection of malignant melanoma is associated with survival rates of up to 90%, but later detection (stage III to stage IV) is associated with survival rates of only 10%. Dysregulation of microRNA (miRNA) expression has been linked to tumor development and progression by functioning either as a tumor suppressor, an oncogene or a metastasis regulator in multiple cancer types. To understand the role of miRNA in the pathogenesis of malignant melanoma and identify biomarkers of metastasis, miRNA expression profiles in skin punches from 33 metastatic melanoma patients and 14 normal healthy donors were compared. We identified a cluster of 14 miRNAs on the X chromosome, termed the miR-506-514 cluster, which was consistently overexpressed in nearly all melanomas tested (30-60 fold, Po0.001), regardless of mutations in N-ras or B-raf. Inhibition of the expression of this cluster as a whole, or one of its sub-clusters (Sub-cluster A) consisting of six mature miRNAs, led to significant inhibition of cell growth, induction of apoptosis, decreased invasiveness and decreased colony formation in soft agar across multiple melanoma cell lines. Sub-cluster A of the miR-506-514 cluster was critical for maintaining the cancer phenotype, but the overexpression of the full cluster was necessary for melanocyte transformation. Our results provide new insights into the functional role of this miRNA cluster in melanoma, and suggest new approaches to treat or diagnose this disease.

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Interplay between small and long non‐coding RNAs in cutaneous melanoma: a complex jigsaw puzzle with missing pieces

et al. 2018

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The incidence of cutaneous melanoma (CM) has increased in the past few decades. The biology of melanoma is characterized by a complex interaction between genetic, environmental and phenotypic factors. A greater understanding of the molecular mechanisms that promote melanoma cell growth and dissemination is crucial to improve diagnosis, prognostication, and treatment of CM. Both small and long non‐coding RNAs (lncRNAs) have been identified to play a role in melanoma biology; microRNA and lncRNA expression is altered in transformed melanocytes and this in turn has functional effects on cell proliferation, apoptosis, invasion, metastasis, and immune response. Moreover, specific dysregulated ncRNAs were shown to have a diagnostic or prognostic role in melanoma and to drive the establishment of drug resistance. Here, we review the current literature on small and lncRNAs with a role in melanoma, with the aim of putting into some order this complex jigsaw puzzle.

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The Promyelocytic Leukemia Zinc Finger–MicroRNA-221/-222 Pathway Controls Melanoma Progression through Multiple Oncogenic Mechanisms

Abstract: The incidence of cutaneous melanoma is steadily increasing.

Cited by 344 publications

References 40 publications

Expression of the promyelocytic leukemia zinc-finger in T-lymphoblastic lymphoma and leukemia has strong implications for their cellular origin and greater association with initial bone marrow involvement

Expression of the promyelocytic leukemia zinc-finger in T-lymphoblastic lymphoma and leukemia has strong implications for their cellular origin and greater association with initial bone marrow involvement

A novel oncogenic role for the miRNA-506-514 cluster in initiating melanocyte transformation and promoting melanoma growth

Interplay between small and long non‐coding RNAs in cutaneous melanoma: a complex jigsaw puzzle with missing pieces

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