RNA-seq of macrophages of amoeboid or mesenchymal migratory phenotype due to specific structure of environment

Čermák, Vladimı́r; Gandalovičová, Aneta; Merta, Ladislav; Fučíková, Jitka; Špíšek, Radek; Rösel, Daniel; Brábek, Jan

doi:10.1038/sdata.2018.198

Cited by 14 publications

(13 citation statements)

References 22 publications

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“…www.nature.com/scientificdata www.nature.com/scientificdata/ statistical analysis. To estimate differential gene expression from RNA sequencing data a workflow based on the STAR aligner and DESeq2 R package was used as described previously 18 . Mass spectrometry data pre-processed with Proteome Discoverer 2.1 were imported into R environment, imputed and normalized with the MSnbase package 33 .…”

Section: Background and Summarymentioning

confidence: 99%

High-throughput transcriptomic and proteomic profiling of mesenchymal-amoeboid transition in 3D collagen

et al. 2020

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The plasticity of cancer cell invasion represents substantial hindrance for effective anti-metastatic therapy. To better understand the cancer cells' plasticity, we performed complex transcriptomic and proteomic profiling of HT1080 fibrosarcoma cells undergoing mesenchymal-amoeboid transition (MAT). As amoeboid migratory phenotype can fully manifest only in 3D conditions, all experiments were performed with 3D collagen-based cultures. Two previously described approaches to induce MAT were used: doxycycline-inducible constitutively active RhoA expression and dasatinib treatment. RNA sequencing was performed with ribo-depleted total RNA. Protein samples were analysed with tandem mass tag (TMT)-based mass spectrometry. The data provide unprecedented insight into transcriptome and proteome changes accompanying MAT in true 3D conditions.

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Section: Background and Summarymentioning

confidence: 99%

High-throughput transcriptomic and proteomic profiling of mesenchymal-amoeboid transition in 3D collagen

et al. 2020

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“…The increased level of MALAT1 after induction of MAT in three distinct cell lines (HT1080 fibrosarcoma cells, MDA-MB-231 breast cancer, and BLM melanoma cell lines) was further experimentally verified by RT-qPCR experiments (Figure 2E,F). It was also previously described in amoeboid macrophages [29].…”

Section: Discussionmentioning

confidence: 64%

“…Furthermore, we analyzed microarray data from constitutively amoeboid A375m2 melanoma cells cultured on top of thick, deformable collagen and treated with ROCK kinase inhibitors Y27632 and H1152 (further referred to as ROCKi) to induce AMT [28]. In addition, we included RNA-seq data from M2 macrophages of either amoeboid or mesenchymal morphology due to different stiffness of the surrounding collagen matrix [29].…”

Section: Comparison Of Transcriptomic Profiles Of Amoeboid Cancer Cells and Macrophages Revealed Upregulation Of Malat1mentioning

confidence: 99%

Increased Level of Long Non-Coding RNA MALAT1 Is a Common Feature of Amoeboid Invasion

Merta

Gandalovičová

Čermák

et al. 2020

Cancers

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The ability of cancer cells to adopt various migration modes (the plasticity of cancer cell invasiveness) is a substantive obstacle in the treatment of metastasis, yet still an incompletely understood process. We performed a comparison of publicly available transcriptomic datasets from various cell types undergoing a switch between the mesenchymal and amoeboid migration modes. Strikingly, lncRNA MALAT1 (metastasis-associated lung adenocarcinoma transcript 1) was one of three genes that were found upregulated in all amoeboid cells analyzed. Accordingly, downregulation of MALAT1 in predominantly amoeboid cell lines A375m2 and A2058 resulted in decrease of active RhoA (Ras homolog family member A) and was accompanied by the amoeboid-mesenchymal transition in A375m2 cells. Moreover, MALAT1 downregulation in amoeboid cells led to increased cell proliferation. Our work is the first to address the role of MALAT1 in MAT/AMT (mesenchymal to amoeboid transition/amoeboid to mesenchymal transition) and suggests that increased MALAT1 expression is a common feature of amoeboid cells.

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“…To estimate differential gene expression from RNA sequencing data, a workflow based on the STAR aligner and DESeq2 R package was used, as described previously [ 65 ]. We used rlog-transformed values for principal component analysis.…”

Section: Methodsmentioning

confidence: 99%

RNA-seq Characterization of Melanoma Phenotype Switch in 3D Collagen after p38 MAPK Inhibitor Treatment

et al. 2021

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Melanoma phenotype plasticity underlies tumour dissemination and resistance to therapy, yet its regulation is incompletely understood. In vivo switching between a more differentiated, proliferative phenotype and a dedifferentiated, invasive phenotype is directed by the tumour microenvironment. We found that treatment of partially dedifferentiated, invasive A375M2 cells with two structurally unrelated p38 MAPK inhibitors, SB2021920 and BIRB796, induces a phenotype switch in 3D collagen, as documented by increased expression of melanocyte differentiation markers and a loss of invasive phenotype markers. The phenotype is accompanied by morphological change corresponding to amoeboid–mesenchymal transition. We performed RNA sequencing with an Illumina HiSeq platform to fully characterise transcriptome changes underlying the switch. Gene expression results obtained with RNA-seq were validated by comparing them with RT-qPCR. Transcriptomic data generated in the study will extend the present understanding of phenotype plasticity in melanoma and its contribution to invasion and metastasis.

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RNA-seq of macrophages of amoeboid or mesenchymal migratory phenotype due to specific structure of environment

Cited by 14 publications

References 22 publications

High-throughput transcriptomic and proteomic profiling of mesenchymal-amoeboid transition in 3D collagen

High-throughput transcriptomic and proteomic profiling of mesenchymal-amoeboid transition in 3D collagen

Increased Level of Long Non-Coding RNA MALAT1 Is a Common Feature of Amoeboid Invasion

RNA-seq Characterization of Melanoma Phenotype Switch in 3D Collagen after p38 MAPK Inhibitor Treatment

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