Migfilin and Mig-2 Link Focal Adhesions to Filamin and the Actin Cytoskeleton and Function in Cell Shape Modulation

Tu, Yizeng; Wu, Shan; Shi, Xiaohua; Chen, Ka; Wu, Chuanyue

doi:10.1016/s0092-8674(03)00163-6

Cited by 331 publications

(463 citation statements)

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“…This finding, together with the previous demonstration that MIG2 is localized to focal adhesions and plays a role in controlling actin cytoskeleton dynamics (15), prompted us to investigate the role of MIG2 in TMX2-28 cell invasion. Using transient transfection of siRNAs targeting MIG2, we silenced MIG2 expression by 52% relative to the negative control (siRNAs targeting glyceraldehyde-3-phosphate dehydrogenase, GAPDH; Fig.…”

Section: Mig2 and Cell Invasion By Tmx2-28 Cellsmentioning

confidence: 83%

“…19), we identified several cell membrane, adhesion, and cell-ECMassociated genes that were up-regulated in TMX2-28 cells (Table 1). MIG2 is localized to focal adhesions and plays a role in controlling actin cytoskeleton dynamics (15); therefore, it is probable that MIG2 plays a role in promoting cell motility and invasion. Tu and colleagues (15) examined the expression of MIG2 in a variety of cell types and found that MIG2 was at a relatively low level in MCF-7 cells.…”

Section: Mig2 Expression In Breast Cancer Cell Linesmentioning

confidence: 99%

“…MIG2 is localized to focal adhesions and plays a role in controlling actin cytoskeleton dynamics (15); therefore, it is probable that MIG2 plays a role in promoting cell motility and invasion. Tu and colleagues (15) examined the expression of MIG2 in a variety of cell types and found that MIG2 was at a relatively low level in MCF-7 cells. We thought it was intriguing that MIG2 was overexpressed in TMX2-28 breast cancer cells; and therefore, further investigated the expression and function of MIG2 in breast cancer.…”

Section: Mig2 Expression In Breast Cancer Cell Linesmentioning

confidence: 99%

“…MIG2 belongs to a newly recognized protein family comprising URP1, URP2 and the Caenorhabditis elegans protein, UNC-112, which all share a unique protein structure consisting of two 4.1-ezrinradixin-moesin domains flanking a pleckstrin homology domain (13,14). MIG2 has been further characterized as a component of cell-ECM adhesion sites and described its involvement in controlling cell shape and spreading (15). Using yeast two-hybrid screening, those authors showed that MIG2 interacts with a recently characterized LIM domaincontaining protein that they termed migfilin (15).…”

Section: Introductionmentioning

confidence: 99%

“…MIG2 has been further characterized as a component of cell-ECM adhesion sites and described its involvement in controlling cell shape and spreading (15). Using yeast two-hybrid screening, those authors showed that MIG2 interacts with a recently characterized LIM domaincontaining protein that they termed migfilin (15). MIG2 recruits migfilin to cell-ECM adhesions, forming a complex with the actin cross-linking protein, filamin, and promoting cellular dynamics through the interaction with the actin cytoskeleton.…”

Section: Introductionmentioning

confidence: 99%

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Use of an Aggressive MCF-7 Cell Line Variant, TMX2-28, to Study Cell Invasion in Breast Cancer

Gozgit

Pentecost

Marconi

et al. 2006

Molecular Cancer Research

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An estrogen receptor -negative variant of the MCF-7 breast cancer cell line, TMX2-28, was used as a model in which to study breast cancer cell invasion. Using a reconstituted basement membrane (Matrigel) assay to evaluate cell invasion, we determined that TMX2-28 cells are more invasive than MCF-7 cells and that the invasiveness of TMX2-28 is similar to that of the aggressive MDA-MB-231 breast cancer cell line. TMX2-28 cells displayed a rounded, epithelial cell -like morphology, suggesting an amoeboid mode of cell invasion, in contrast to the mesenchymal mode of invasion characteristic of spindle-shaped, fibroblast-like MDA-MB-231 cells. Using real-time reverse transcription-PCR, we found that mitogen-inducible gene 2 (MIG2) is expressed at a 17-fold higher level in TMX2-28 cells than in nonaggressive MCF-7 cells and that MIG2 mRNA levels are low in the nontumorigenic human mammary epithelial cell line, 184. We determined that MIG2 plays a role in cell invasion by using small interfering RNA (siRNA) to suppress the expression of MIG2 mRNA levels in TMX2-28 cells. TMX2-28 cell invasion was reduced by 48% when the cells were transfected with siRNAs targeting MIG2, relative to cells transfected with siRNAs against glyceraldehyde-3-phosphate dehydrogenase. Finally, MIG2 expression was evaluated in reductive mammoplasty and breast tumor tissue. Although all 21 normal tissues from reduction mammoplasty showed immunoreactivity for MIG2, ranging from weak (62%) to strong (24%), only half of the 34 formalin-fixed breast tumors showed immunoreactivity for MIG2. Of these 17 positive cases, 10 were considered to overexpress MIG2 (moderate to strong staining). Examination of 30 frozen breast tumors supported the finding that MIG2 is overexpressed in a subset of breast cancers. We suggest that MIG2's normal regulation and function are disrupted in breast cancer. (Mol Cancer Res 2006;4(12):905 -13)

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Section: Mig2 and Cell Invasion By Tmx2-28 Cellsmentioning

confidence: 83%

Section: Mig2 Expression In Breast Cancer Cell Linesmentioning

confidence: 99%

Section: Mig2 Expression In Breast Cancer Cell Linesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Use of an Aggressive MCF-7 Cell Line Variant, TMX2-28, to Study Cell Invasion in Breast Cancer

Gozgit

Pentecost

Marconi

et al. 2006

Molecular Cancer Research

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Genetic Basis of Developmental Malformations of the Cerebral Cortex

Mochida¹,

Walsh²

2004

Arch Neurol

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Widespread use of noninvasive brain imaging techniques, in particular magnetic resonance imaging, has led to increased recognition of genetic disorders of cortical development in recent years. The causative genes for many of these disorders have been identified through a combination of detailed clinical and radiological analyses and molecular genetic approaches. These disease genes have been found to affect different steps of cortical development, including proliferation of neuronal progenitor cells, neuronal migration, and maintaining integrity of the pial surface. In many cases, syndromes with similar clinical phenotypes are caused by genes with related biochemical functions. In this article, we review the recent advances in molecular genetic studies of the disorders of cortical development. The identification and functional studies of the genes associated with these developmental disorders will likely lead to improvement in diagnosis and facilitate our understanding of the mechanisms of cortical development.

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Associations of the Top 20 Alzheimer Disease Risk Variants With Brain Amyloidosis

et al. 2018

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IMPORTANCE Late-onset Alzheimer disease (AD) is highly heritable. Genome-wide association studies have identified more than 20 AD risk genes. The precise mechanism through which many of these genes are associated with AD remains unknown. OBJECTIVE To investigate the association of the top 20 AD risk variants with brain amyloidosis. DESIGN, SETTING, AND PARTICIPANTS This study analyzed the genetic and florbetapir F 18 data from 322 cognitively normal control individuals, 496 individuals with mild cognitive impairment, and 159 individuals with AD dementia who had genome-wide association studies and 18F-florbetapir positron emission tomographic data from the Alzheimer’s Disease Neuroimaging Initiative (ADNI), a prospective, observational, multisite tertiary center clinical and biomarker study. This ongoing study began in 2005. MAIN OUTCOMES AND MEASURES The study tested the association of AD risk allele carrier status (exposure) with florbetapir mean standard uptake value ratio (outcome) using stepwise multivariable linear regression while controlling for age, sex, and apolipoprotein E ε4 genotype. The study also reports on an exploratory 3-dimensional stepwise regression model using an unbiased voxelwise approach in Statistical Parametric Mapping 8 with cluster and significance thresholds at 50 voxels and uncorrected P < .01. RESULTS This study included 977 participants (mean [SD] age, 74 [7.5] years; 535 [54.8%] male and 442 [45.2%] female) from the ADNI-1, ADNI-2, and ADNI–Grand Opportunity. The adenosine triphosphate–binding cassette subfamily A member 7 (ABCA7) gene had the strongest association with amyloid deposition (χ2 = 8.38, false discovery rate–corrected P < .001), after apolioprotein E ε4. Significant associations were found between ABCA7 in the asymptomatic and early symptomatic disease stages, suggesting an association with rapid amyloid accumulation. The fermitin family homolog 2 (FERMT2) gene had a stage-dependent association with brain amyloidosis (FERMT2 × diagnosis χ2 = 3.53, false discovery rate–corrected P = .05), which was most pronounced in the mild cognitive impairment stage. CONCLUSIONS AND RELEVANCE This study found an association of several AD risk variants with brain amyloidosis. The data also suggest that AD genes might differentially regulate AD pathologic findings across the disease stages.

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Migfilin and Mig-2 Link Focal Adhesions to Filamin and the Actin Cytoskeleton and Function in Cell Shape Modulation

Cited by 331 publications

References 51 publications

Use of an Aggressive MCF-7 Cell Line Variant, TMX2-28, to Study Cell Invasion in Breast Cancer

Use of an Aggressive MCF-7 Cell Line Variant, TMX2-28, to Study Cell Invasion in Breast Cancer

Genetic Basis of Developmental Malformations of the Cerebral Cortex

Associations of the Top 20 Alzheimer Disease Risk Variants With Brain Amyloidosis

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