LIMCH1 regulates nonmuscle myosin-II activity and suppresses cell migration

Lin, Yu‐Hung; Zhen, Yen-Yi; Chien, Kun-Yi; Lee, I-Ching; Lin, Wei; Chen, Meiyu; Pai, Li‐Mei

doi:10.1091/mbc.e15-04-0218

Cited by 49 publications

(53 citation statements)

References 60 publications

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“…As a proof of principle, here we focused on LIMCH1 as a key regulator of stress fiber formation and AC remodeling. Whereas previous studies already demonstrated the active role of this and other genes in stress fiber formation (Koyama & Baba, 1996;Lin et al, 2017), our data further extend these findings and reveal the surprising discovery of a direct regulation by Nup93. It is important to highlight that we cannot exclude the possibility that another protein localized between Nup93 and the DNA might also be involved in this regulation.…”

Section: Discussionsupporting

confidence: 88%

“…Both these genes could be involved in the observed AC remodeling and stress fiber formation. In particular, LIMCH1 is an actin-related protein whose deletion was associated with decreased stress fibers, reduced focal adhesions, and increased cell migration (Lin et al, 2017). To test the functional significance of LIMCH1 in the context of triple-negative, claudin-low BCCs, we simultaneously depleted Nup93 and LIMCH1 (Fig 4C) with the final goal to verify if this double deletion could partially revert the phenotype of NUP93-silenced cells.…”

Section: Nup93 Directly Regulates Genes Associated With Ecm/cytoskelementioning

confidence: 99%

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Nup93 regulates breast tumor growth by modulating cell proliferation and actin cytoskeleton remodeling

et al. 2020

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Nucleoporin 93 (Nup93) expression inversely correlates with the survival of triple-negative breast cancer patients. However, our knowledge of Nup93 function in breast cancer besides its role as structural component of the nuclear pore complex is not understood. Combination of functional assays and genetic analyses suggested that chromatin interaction of Nup93 partially modulates the expression of genes associated with actin cytoskeleton remodeling and epithelial to mesenchymal transition, resulting in impaired invasion of triple-negative, claudin-low breast cancer cells. Nup93 depletion induced stress fiber formation associated with reduced cell migration/proliferation and impaired expression of mesenchymal-like genes. Silencing LIMCH1, a gene responsible for actin cytoskeleton remodeling and up-regulated upon Nup93 depletion, partially restored the invasive phenotype of cancer cells. Loss of Nup93 led to significant defects in tumor establishment/propagation in vivo, whereas patient samples revealed that high Nup93 and low LIMCH1 expression correlate with late tumor stage. Our approach identified Nup93 as contributor of triple-negative, claudin-low breast cancer cell invasion and paves the way to study the role of nuclear envelope proteins during breast cancer tumorigenesis.

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Section: Discussionsupporting

confidence: 88%

Section: Nup93 Directly Regulates Genes Associated With Ecm/cytoskelementioning

confidence: 99%

Nup93 regulates breast tumor growth by modulating cell proliferation and actin cytoskeleton remodeling

et al. 2020

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“…Indeed, cell contraction accelerates when LIMCH1 promotes the assembly of actin stress fibres during cell spreading. Moreover, the absence of LIMCH1 expression impacts the formation of actin stress fibres as well as the stability of focal adhesions (Lin et al 2017), which are fundamental structures in the union of muscle fibres to ensure optimal contraction and muscular distention. TIGD4 protein belongs to the tigger subfamily of the pogo superfamily of DNA-mediated transposons in humans.…”

Section: Micementioning

confidence: 99%

Muscle molecular adaptations to endurance exercise training are conditioned by glycogen availability: a proteomics‐based analysis in the McArdle mouse model

Fiuza‐Luces

Santos‐Lozano

Llavero

et al. 2018

The Journal of Physiology

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McArdle's disease is an inborn disorder of skeletal muscle glycogen metabolism that results in blockade of glycogen breakdown due to mutations in the myophosphorylase gene. We recently developed a mouse model carrying the homozygous p.R50X common human mutation (McArdle mouse), facilitating the study of how glycogen availability affects muscle molecular adaptations to endurance exercise training. Using quantitative differential analysis by liquid chromatography with tandem mass spectrometry, we analysed the quadriceps muscle proteome of 16-week-old McArdle (n = 5) and wild-type (WT) (n = 4) mice previously subjected to 8 weeks' moderate-intensity treadmill training or to an equivalent control (no training) period. Protein networks enriched within the differentially expressed proteins with training in WT and McArdle mice were assessed by hypergeometric enrichment analysis. Whereas endurance exercise training improved the estimated maximal aerobic capacity of both WT and McArdle mice as compared with controls, it was ∼50% lower than normal in McArdle mice before and after training. We found a remarkable difference in the protein networks involved in muscle tissue adaptations induced by endurance exercise training with and without glycogen availability, and training induced the expression of only three proteins common to McArdle and WT mice: LIM and calponin homology domains-containing protein 1 (LIMCH1), poly (ADP-ribose) polymerase 1 (PARP1 - although the training effect was more marked in McArdle mice), and tigger transposable element derived 4 (TIGD4). Trained McArdle mice presented strong expression of mitogen-activated protein kinase 12 (MAPK12). Through an in-depth proteomic analysis, we provide mechanistic insight into how glycogen availability affects muscle protein signalling adaptations to endurance exercise training.

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“…In a microarray screen to identify genes downregulated in tfap2a/g-deficient zebrafish embryos, formation and actomyosin dynamics (Lin et al, 2017). Lmo7 can localize to FAs and act as a shuttling 95 protein to mediate integrin signaling in HeLa cells and mouse embryonic fibroblasts (Holaska et al, 2006;96 Wozniak et al, 2013).…”

Section: Fates 74mentioning

confidence: 99%

Lmo7a Coordinates Neural Crest Migration and Lineage Specification by Regulating Cell Adhesion Dynamics

Tatarakis

Tuttle

2020

Preprint

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22Cell migration requires dynamic regulation of cell-cell signaling and cell adhesion. Neural crest (NC) cells 23 are highly migratory cells, which undergo an epithelial-mesenchymal transition (EMT) to leave the neural 24 epithelium and migrate throughout the body to give rise to many different derivatives. We have identified 25 a Lim-domain only (Lmo) protein, Lmo7a, expressed in early NC cells that controls both actin cytoskeletal 26 dynamics and Wnt signaling during NC migration. In embryos deficient in Lmo7a, many NC cells fail to 27 migrate away from the dorsal midline, and form aggregates. Unlike the majority of NC cells that appear to 28 migrate normally, cells that aggregate in Lmo7a-deficient embryos mislocalize paxillin (Pxn) and have 29 reduced levels of phosphorylated focal adhesion kinase (pFAK). Lmo7a loss-of-function also disrupts 30canonical Wnt signaling such that after the onset of NC cell migration, Wnt responses and nuclear β-31 catenin levels increase in the cells that aggregate. However, this increase in Wnt signaling appears 32 secondary to the defect in migration. Similar to mutants for other Wnt regulators in NC cells, the NC cells 33in Lmo7a-deficient aggregates exhibit gene expression signatures of pigment cell progenitors, but also 34 express markers of Schwann cell progenitors, suggesting a role for Lmo7a in pigment-glial specification. 35We propose that Lmo7a modulates cell adhesion to facilitate both robust NC cell migration and a subset 36 of lineage decisions.

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LIMCH1 regulates nonmuscle myosin-II activity and suppresses cell migration

Cited by 49 publications

References 60 publications

Nup93 regulates breast tumor growth by modulating cell proliferation and actin cytoskeleton remodeling

Nup93 regulates breast tumor growth by modulating cell proliferation and actin cytoskeleton remodeling

Muscle molecular adaptations to endurance exercise training are conditioned by glycogen availability: a proteomics‐based analysis in the McArdle mouse model

Lmo7a Coordinates Neural Crest Migration and Lineage Specification by Regulating Cell Adhesion Dynamics

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