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Live Quantitative Phase Imaging

Live quantitative imaging was performed using either the HoloMonitor M4 imaging cytometers (Phase Holographic Imaging, Lund, Sweden) or the Livecyte platform (Phasefocus, Sheffield, UK). 

Analyses of cell proliferation, dry cell mass, and death were acquired with the M4 platform and analyzed using HStudio (v2.6.3) as previously described. For each experiment, human melanocytes were seeded into 6-well plates (Sarstedt, 83.3920) at 100,000 cells/well and either live-imaged or serially imaged as indicated. 

Analysis of growth rate were acquired with the M4 platform and analyzed using App Suite (v3.2.0.60) as previously described. For each experiment, 100,000 melanocytes, 60,000 501Mel cells or 150,000 HCIMel019 cells were plated per well and media containing indicated concentrations of barasertib (AURKB inhibitor; AZD1152-HQPA | AZD2811, Selleckchem, A1147) was added. 

Cells were imaged for 48-72 hours. Analyses of fluorescent reporters coupled with quantitative phase imaging was conducted using the Livecyte platform and analyzed using Analyze (v3.1) (Phasefocus, Sheffield, UK).

Tillägg.Rätt svar har kommit in via kommentarsfältet. Och visst är det en studie om hudcancer Robert L.Judson-Torres et al har åstadkommit.

MicroRNAs Restrain Proliferation in BRAF^V600E Melanocytic Nevi

Abstract

Benign melanocytic nevi commonly form when melanocytes that acquire a BRAF^V600E mutation undergo a period of rapid proliferation and subsequent arrest. Constitutive activation of MAPK signaling downstream of BRAF drives the initial proliferative phenotype. However, the factors that establish and maintain growth arrest in nevi remain elusive. The growth-arrested state of BRAF^V600E melanocytes is not conferred by additional genetic mutations, suggesting a role for regulatory elements. We investigated the role of microRNAs in the initiation and maintenance of nevus arrest. Using primary human melanocytes, melanocytic nevi, and adjacent melanoma, we show that MIR211-5p and MIR328-3p are enriched in nevi compared to normal melanocytes, then subsequently downregulated in adjacent melanoma. Both MIR211-5p and MIR328-3p proved necessary effectors of BRAF^V600E-induced growth arrest in human melanocytes. We identified microRNA target networks which, when suppressed, phenocopy BRAF^V600E-induced arrest and converge on inhibition of AURKB to block cell cycle progression in primary human melanocytes.

Statement of Significance We describe a microRNA regulatory network that enforces BRAF^V600E-induced growth arrest in human melanocytes during melanocytic nevus formation. De-regulation of MIR211-5p and MIR328-3p targets – which converge on AURKB – leads to cell cycle re-entry and melanoma progression. AURKB inhibition therefore provides a potential therapeutic intervention for melanoma prevention or treatment.

 

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