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Secretion of interleukin-1 by dedifferentiated melanoma cells inhibits JAK1-STAT3-driven actomyosin contractility of lymph node fibroblastic reticular cells

ABSTRACT: Secretion of interleukin-1 by dedifferentiated melanoma cells inhibits JAK1-STAT3-driven actomyosin contractility of lymph node fibroblastic reticular cells

PROVIDER: PRJNA661045 | ENA |

REPOSITORIES: ENA

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Secretion of interleukin-1 by dedifferentiated melanoma cells inhibits JAK1-STAT3-driven actomyosin contractility of lymph node fibroblastic reticular cells

Project description:Fibroblastic reticular cells (FRC) are immunologically specialized myofibroblasts that control the elasticity of the lymph node (LN), in part through their contractile properties. Swelling of tumor-draining LN is a hallmark of lymphophilic cancers such as cutaneous melanoma. Melanoma displays high intratumoral heterogeneity with the coexistence of melanoma cells with variable differentiation phenotypes, from melanocytic to dedifferentiated states. Factors secreted by melanoma cells promote pre-metastatic LN reprograming and tumor spreading. Elucidating the impact of the melanoma secretome on FRC could help identify approaches to prevent metastasis. Here we show that melanocytic and dedifferentiated melanoma cells differentially impact the FRC contractile phenotype. Factors secreted by dedifferentiated cells, but not by melanocytic cells, strongly inhibited actomyosin-dependent contractile forces of FRC by decreasing the activity of the RHOA-ROCK pathway and the mechano-responsive transcriptional co-activator YAP. Transcriptional profiling and biochemical analyses indicated that actomyosin cytoskeleton relaxation in FRC is driven by inhibition of the JAK1-STAT3 pathway. This FRC relaxation was associated with increased FRC proliferation and activation and with elevated tumor invasion in vitro. The secretome of dedifferentiated melanoma cells also modulated the biomechanical properties of distant LN in pre-metastatic mouse models. Lastly, interleukin-1 produced by dedifferentiated cells was involved in the inhibition of FRC contractility. These data highlight the role of the JAK1-STAT3 and YAP pathways in spontaneous contractility of resting FRC. They also suggest that dedifferentiated melanoma cells specifically target FRC biomechanical properties to favor tumor spreading in the pre-metastatic LN niche. Targeting this remote communication could be an effective strategy to prevent metastatic spread of the disease.

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Expression data from actomyosin contractility regulated genes

Project description:Actomyosin contractility regulates cell morphology and movement. The objective of this study was to identify whether actomyosin contractility regulates gene expression in tumour cells and whether such genes are involved in cell morphology and movement. Gene expression analysis was carried out on highly contractile melanoma cell line A375M2 plated on a deformable collagen matrix under conditions where actomyosin contractility could be altered following treatment with blebbistatin, a direct inhibitor of myosin II, or Rho-kinase inhibitors Y27632 or H1152 that interfere with signalling to myosin II. 18 samples (6 x 3 biological replicates). Cells were plated on rigid or deformable matrices. Rounded cells (A375M2 melanoma cells) plated on deformable matrices were left untreated or treated with Rho-kinase inhibitors Y27632, H1152 or blebbistatin an inhibitor of mysoin II.

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Expression data from actomyosin contractility regulated genes

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Linking planar polarity signaling directly to actomyosin contractility during vertebrate neurulation

Project description:Actomyosin contractility represents an ancient feature of eukaryotic cells participating in many developmental and homeostasis events, including tissue morphogenesis, muscle contraction, and cell migration, with dysregulation implicated in various pathological conditions, such as cancer. At the molecular level, actomyosin comprises actin bundles and myosin motor proteins that are sensitive to posttranslational modifications like phosphorylation. While the molecular components of actomyosin and its regulation are well understood, the coordination of contractility by extracellular and intracellular signals, particularly from cellular signaling pathways, remains incompletely elucidated. This study focuses on planar cell polarity (PCP) signaling, previously associated with actomyosin contractility during vertebrate neurulation. Contrary to previous studies, our investigation reveals that main cytoplasmic PCP proteins, Prickle and Dishevelled, interact directly with key actomyosin components such as myosin light chain (MLC), leading to its phosphorylation and localized activation. Through relevant in vitro and in vivo models, we demonstrate that these PCP proteins function not merely passively and indirectly as previously reported, but that they actively control actomyosin contractility by acting as scaffold proteins, orchestrating the necessary machinery for contractility. These findings unveil a direct link of PCP signaling in crucial actomyosin contractility processes through MLC that are relevant to vertebrate neurulation and potentially beyond.

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Top-Down Individual Ion Mass Spectrometry Reveals 85-110 kDa Catenin Phospho-Proteoforms Regulated by Actomyosin Contractility

Project description:Data associated with the manuscript "Top-Down Individual Ion Mass Spectrometry Reveals 85-110 kDa Catenin Phospho-Proteoforms Regulated by Actomyosin Contractility"

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Gene array data of tumour draining lymph node fibroblastic reticular cells (FRCs)

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Aldh1a2+ fibroblastic reticular cells regulate lymphocyte recruitment in omental milky spots

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