mi<scp>RNA</scp> in mycosis fungoides and skin inflammation

Persson, Jenny L.

doi:10.1111/apm.12186

Cited by 11 publications

(8 citation statements)

References 30 publications

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“…74 MicroRNA (miRNA, miR) are small, non-coding RNA molecules that regulate gene expression at the post-transcriptional level by targeting the 3’-untranslated regions of messenger RNA to promote their degradation or decrease their translation. 75 Several studies have identified different miRNA signatures for CD30 + pcALCL. 62,76–78 Benner et al .…”

Section: Primary Cutaneous Anaplastic Large Cell Lymphomamentioning

confidence: 99%

CD30-positive primary cutaneous lymphoproliferative disorders: molecular alterations and targeted therapies

Prieto‐Torres¹,

Rodríguez‐Pinilla

Onaindía

et al. 2019

Haematologica

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Primary cutaneous CD30-positive T-cell lymphoproliferative disorders are the second most common subgroup of cutaneous T-cell lymphomas. They include two clinically different entities with some overlapping features and borderline cases: lymphomatoid papulosis and primary cutaneous anaplastic large cell lymphoma. Molecular studies of primary cutaneous anaplastic large cell lymphoma reveal an increasing level of heterogeneity that is associated with histological and immunophenotypic features of the cases and their response to specific therapies. Here, we review the most significant genetic, epigenetic and molecular alterations described to date in primary cutaneous CD30-positive T-cell lymphoproliferative disorders, and their potential as therapeutic targets.

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Section: Primary Cutaneous Anaplastic Large Cell Lymphomamentioning

confidence: 99%

CD30-positive primary cutaneous lymphoproliferative disorders: molecular alterations and targeted therapies

Prieto‐Torres¹,

Rodríguez‐Pinilla

Onaindía

et al. 2019

Haematologica

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“…However, the modus operandi of this switch to malignant inflammation is not fully understood. Recently, microRNAs were implicated in CTCL pathogenesis, progression, and prognosis (Kopp et al, 2013;Persson, 2013;Ralfkiaer et al, 2011;Ralfkiaer et al, 2014;: microRNA (miR)-155 and miR-21, which are induced by deregulated JAK3/STAT signaling, appear to be key players, because their aberrant expression in situ is associated with disease progression. However, little is known about their downstream targets and function in malignant T cells.…”

Section: Introductionmentioning

confidence: 99%

SATB1 in Malignant T Cells

Fredholm

Willerslev-Olsen

Met

et al. 2018

Journal of Investigative Dermatology

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Deficient expression of SATB1 hampers thymocyte development and results in inept T-cell lineages. Recent data implicate dysregulated SATB1 expression in the pathogenesis of mycosis fungoides, the most frequent variant of cutaneous T-cell lymphoma. Here, we report on a disease stage-associated decrease of SATB1 expression and an inverse expression of STAT5 and SATB1 in situ. STAT5 inhibited SATB1 expression through induction of microRNA-155. Decreased SATB1 expression triggered enhanced expression of IL-5 and IL-9 (but not IL-6 and IL-32), whereas increased SATB1 expression had the opposite effect, indicating that the microRNA-155 target SATB1 is a repressor of IL-5 and IL-9 in malignant T cells. In accordance, inhibition of STAT5 and its upstream activator JAK3 triggered increased SATB1 expression and a concomitant suppression of IL-5 and IL-9 expression in malignant T cells. In conclusion, we provide a mechanistic link between the proto-oncogenic JAK3/STAT5/microRNA-155 pathway, SATB1, and cytokines linked to CTCL severity and progression, indicating that SATB1 dysregulation is involved in cutaneous T-cell lymphoma pathogenesis.

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“…Other targets of miR-181b include the oncogenes Tcl-1 and Mcl-1 , with low expression of miR-181b in these CLL patients correlating with poor prognosis [31, 39, 48]. In CTCL, miRs may also contribute to chemotherapy-induced apoptosis, aberrant cytokine expression, and impaired immune responses [49]. MiR-181a and miR-181b in particular were recently found to be significantly upregulated in CTCL patients, with implications in prognosis for patients with this profile [45].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-181 contributes to downregulation of SAMHD1 expression in CD4+ T-cells derived from Sèzary syndrome patients

et al. 2017

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Sézary syndrome (SS) is a rare subtype of cutaneous T-cell lymphoma (CTCL) that is characterized by aggressive spread of neoplastic CD4+ T-cells from the skin into the bloodstream with metastasis to visceral organs. The deoxynucleoside triphosphohydrolase SAMHD1 is highly expressed in normal CD4+ T-cells, while its expression is down-regulated in CD4+ T-cells from SS patients. MicroRNA (miR) dysregulation is an important epigenetic mechanism in the pathogenesis and progression of SS. MiR-181 has been shown to inhibit SAMHD1 expression in cell lines and was identified as an important prognostic biomarker in CTCL. However, whether SAMHD1 is down-regulated by miR-181 in primary CD4+ T-cells of SS patients is unknown. Compared to normal CD4+ T-cells, SAMHD1 protein expression is significantly reduced in transformed CD4+ T-cell lines and CD4+ T-cells from SS patients, which inversely correlates with increased miR-181 levels in these cells. Over-expression of miR-181b in primary CD4+ T-cells from healthy donors significantly decreased SAMHD1 protein level, but not mRNA level. In contrast, inhibition of miR-181 in a CD4+ T-cell line significantly increased the level of SAMHD1 protein expression. Our results demonstrate that miR-181 is an important regulator of SAMHD1 protein expression in neoplastic CD4+ T-cells, likely through a mechanism of translational inhibition.

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miRNA in mycosis fungoides and skin inflammation

Cited by 11 publications

References 30 publications

CD30-positive primary cutaneous lymphoproliferative disorders: molecular alterations and targeted therapies

CD30-positive primary cutaneous lymphoproliferative disorders: molecular alterations and targeted therapies

SATB1 in Malignant T Cells

MicroRNA-181 contributes to downregulation of SAMHD1 expression in CD4+ T-cells derived from Sèzary syndrome patients

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