The histone code reader Spin1 controls skeletal muscle development

Greschik, Holger; Duteil, Delphine; Messaddeq, Nadia; Willmann, Dominica; Arrigoni, Laura; Sum, Manuela; Jung, Manfred; Metzger, Daniel; Günther, Thomas; Schüle, Roland

doi:10.1038/cddis.2017.468

Cited by 15 publications

(10 citation statements)

References 69 publications

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“… 40 SPIN1 has also been shown to function as a histone code reader to control skeletal muscle functional networks. 41 In this work, we found that the miR-409/SPIN1 axis could regulate cell migration and proliferation in NSCLC cells through the PI3K/AKT pathway. We also identified that the SPIN1 overexpression directly promoted NSCLC progression.…”

Section: Discussionmentioning

confidence: 77%

miR-409 Inhibits Human Non-Small-Cell Lung Cancer Progression by Directly Targeting SPIN1

Song

Xiao

et al. 2018

Molecular Therapy - Nucleic Acids

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Lung cancers, the leading cause of cancer mortality worldwide, are characterized by a high metastatic potential. Growing evidence reveals that Spindlin 1 (SPIN1) is involved in tumor progression and carcinogenesis. However, the role of SPIN1 in non-small-cell lung cancer (NSCLC) and the molecular mechanisms underlying SPIN1 in human NSCLC remain undetermined. Here we examined the function of SPIN1 in human NSCLC and found that the expression of SPIN1 was closely correlated with the overall survival and poor prognosis of NSCLC patients. Aberrant regulation of microRNAs (miRNAs) has an important role in cancer progression. We revealed that miR-409 inhibits the expression of SPIN1 by binding directly to the 3′ UTR of SPIN1 using dual-luciferase reporter assays. Overexpression of miR-409 significantly suppressed cell migration, growth, and proliferation by inhibiting SPIN1 in vitro and in vivo. SPIN1 overexpression in miR-409-transfected NSCLC cells effectively rescued the suppression of cell migration, growth, and proliferation regulated by miR-409. miR-409 regulates the PI3K/AKT (protein kinase B) pathway in NSCLC. Moreover, clinical data showed that NSCLC patients with high levels of miR-409 experienced significantly better survival. miR-409 expression was also negatively associated with SPIN1 expression. Taken together, these findings highlight that the miR-409/SPIN1 axis is a useful pleiotropic regulatory network and could predict the metastatic potential in NSCLC patients early, indicating the possibility that miR-409 and SPIN1 might be attractive prognostic markers for treating NSCLC patients.

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Section: Discussionmentioning

confidence: 77%

miR-409 Inhibits Human Non-Small-Cell Lung Cancer Progression by Directly Targeting SPIN1

Song

Xiao

et al. 2018

Molecular Therapy - Nucleic Acids

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“…Aging is complex set of genetic [40,41], epigenetic [42–46], immunological [47–51], and metabolic [52–58] rearrangements, involving several cellular signalling pathways [59–63] able to regulate metabolism, ROS formation [64–71] and DNA Damage Response (DDR) [72–74] in all organs [75–77]. Therefore, the identification of novel pathways involving p53-mediated responses [78,79] is of crucial interest.…”

Section: Discussionmentioning

confidence: 99%

ZNF185 is a p53 target gene following DNA damage

Smirnov

Cappello

Lena

et al. 2018

Aging

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The transcription factor p53 is a key player in the tumour suppressive DNA damage response and a growing number of target genes involved in these pathways has been identified. p53 has been shown to be implicated in controlling cell motility and its mutant form enhances metastasis by loss of cell directionality, but the p53 role in this context has not yet being investigated. Here, we report that ZNF185, an actin cytoskeleton-associated protein from LIM-family of Zn-finger proteins, is induced following DNA-damage. ChIP-seq analysis, chromatin crosslinking immune-precipitation experiments and luciferase assays demonstrate that ZNF185 is a bona fide p53 target gene. Upon genotoxic stress, caused by DNA-damaging drug etoposide and UVB irradiation, ZNF185 expression is up-regulated and in etoposide-treated cells, ZNF185 depletion does not affect cell proliferation and apoptosis, but interferes with actin cytoskeleton remodelling and cell polarization. Bioinformatic analysis of different types of epithelial cancers from both TCGA and GTEx databases showed a significant decrease in ZNF185 mRNA level compared to normal tissues. These findings are confirmed by tissue micro-array IHC staining. Our data highlight the involvement of ZNF185 and cytoskeleton changes in p53-mediated cellular response to genotoxic stress and indicate ZNF185 as potential biomarker for epithelial cancer diagnosis.

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“…Myf5-Cre line we employed has been previously used to examine satellite cells in limb and extraocular muscles, to ablate embryonic myogenic cells, and to conditionally ablate genes in skeletal muscle (Comai et al, 2014;Gensch et al, 2008;Greschik et al, 2017;Kuang et al, 2007;Stuelsatz et al, 2014). We note that the Myf5-Cre allele may not be effecting a full deletion of Pbx1 in all myoblasts ( Fig.…”

Section: Discussionmentioning

confidence: 99%

Evolutionarily conserved regulation of embryonic fast-twitch skeletal muscle differentiation by Pbx factors

Farr¹,

Risolino

et al. 2020

Preprint

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Vertebrate skeletal muscles are composed of both slow-twitch and fast-twitch fiber types. How the differentiation of distinct fiber types is activated during embryogenesis is not well characterized. Skeletal muscle differentiation is initiated by the activity of the myogenic basic helix-loop-helix (bHLH) transcription factors Myf5, Myod1, Myf6, and Myog. Myod1 functions as a muscle master regulatory factor and directly activates muscle differentiation genes, including those specific to both slow and fast muscle fibers. Our previous studies showed that Pbx TALE-class homeodomain proteins bind with Myod1 on the promoter of the zebrafish fast muscle gene mylpfa and are required for proper activation of mylpfa expression and the fasttwitch muscle-specific differentiation program in zebrafish embryos. Pbx proteins have also been shown to bind regulatory regions of muscle differentiation genes in mammalian muscle cells in culture. Here, we use new zebrafish mutant strains to confirm the essential roles of zebrafish Pbx factors in embryonic fast muscle differentiation. Furthermore, we examine the requirements for Pbx genes in mouse embryonic skeletal muscle differentiation, an area that has not been investigated in the mammalian embryo. Removing Pbx1 function from skeletal muscle in Myf5 Cre/+; Pbx1 fl/fl mouse embryos has minor effects on embryonic muscle development.However, concomitantly deleting Pbx2 function in Myf5 Cre/+ ;Pbx1 fl/fl ;Pbx2 -/mouse embryos causes delayed activation and reduced expression of fast muscle differentiation genes. In the mouse, Pbx1/Pbx2-dependent fast muscle genes closely match those that have been previously shown to be dependent on murine Six1 and Six4. This work establishes evolutionarily conserved requirements for Pbx factors in embryonic fast muscle differentiation. Our studies are revealing how Pbx homeodomain proteins help direct specific cellular differentiation pathways.

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The histone code reader Spin1 controls skeletal muscle development

Cited by 15 publications

References 69 publications

miR-409 Inhibits Human Non-Small-Cell Lung Cancer Progression by Directly Targeting SPIN1

miR-409 Inhibits Human Non-Small-Cell Lung Cancer Progression by Directly Targeting SPIN1

ZNF185 is a p53 target gene following DNA damage

Evolutionarily conserved regulation of embryonic fast-twitch skeletal muscle differentiation by Pbx factors

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