Gelsolin affects the migratory ability of human colon adenocarcinoma and melanoma cells

Litwin, Monika; Nowak, Dorota; Mazur, Antonina Joanna; Baczyńska, Dagmara; Mannherz, Hans Georg; Malicka-Błaszkiewicz, Maria

doi:10.1016/j.lfs.2012.03.039

Cited by 29 publications

(30 citation statements)

References 37 publications

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“…High level of gelsolin as well as its relocation to the sub-membranous region of the cell may directly contribute to the dynamic actin cytoskeletal reorganization in the response to lumican. In addition, in our studies we have observed differences in the gelsolin expression level between normal and cancer cells [57]. There are numerous data showing that the level of gelsolin in different types of cancer cells may change during metastasis [27,28,[58][59][60].…”

Section: Discussionsupporting

confidence: 55%

“…We previously showed that increased level of gelsolin expression leads to its relocation to the sub-membranous region of the cell, followed by distinct changes in the state of actin polymerization and an increase in the migratory abilities of the human colon adenocarcinoma cells. In LS180 cells overexpressing gelsolin we observed vinculin redistribution and its colocalization with gelsolin [57]. Recent data indicate that vinculin, despite its structural role in anchoring actin filaments in the cytoplasmic membrane, participates also in the formation of podosomes [32,56].…”

Section: Discussionmentioning

confidence: 64%

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Overexpression of lumican affects the migration of human colon cancer cells through up-regulation of gelsolin and filamentous actin reorganization

Radwańska

Litwin

Nowak

et al. 2012

Experimental Cell Research

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Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 64%

Overexpression of lumican affects the migration of human colon cancer cells through up-regulation of gelsolin and filamentous actin reorganization

Radwańska

Litwin

Nowak

et al. 2012

Experimental Cell Research

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“…Gelsolin has two subtypes, intracellular gelsolin (cGSN) and plasma gelsolin (pGSN). cGSN has been reported to play important roles in the regulation of cell apoptosis, tumor progression, phagocytosis, actin activity regulation, blood platelet formation, and cell movement [19,20,21,22,23,24,25,26,27]. pGSN plays important roles in body protection and internal environment stability as one of the most important actin-binding proteins in the actin-clearing system.…”

Section: Discussionmentioning

confidence: 99%

Plasma Gelsolin Induced Glomerular Fibrosis via the TGF-β1/Smads Signal Transduction Pathway in IgA Nephropathy

Zhang

Han

et al. 2017

IJMS

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Glomerular fibrosis has been shown to be closely related to the progression and prognosis of IgA nephropathy (IgAN). However, mechanism underlying IgAN glomerular fibrosis remains unclear. Recently, our study showed that plasma gelsolin (pGSN) was decreased in the serum of an IgAN mouse model and that pGSN deposition was found in the glomeruli. Another cytokine, TGF-β1, which is closely related to glomerular fibrosis, was also found to be highly expressed in the glomeruli. In the present study, we report that pGSN induces glomerular fibrosis through the TGF-β1/Smads signal transduction pathway. This is supported by the following findings: human mesangial cells (HMCs) show remarkable morphological changes and proliferation in response to co-stimulation with pGSN and polymeric IgA1 (pIgA1) from IgAN patients compared to other controls. Moreover, ELISA assays showed that more TGF-β1 secretion was found in HMCs supernatants in the co-stimulation group. Further experiments showed increased TGF-β1, Smad3, p-Smad2/3, Smad4, and collagen 1 and decreased Smad7 expression in the co-stimulation group. Our present study implied that the synergistic effect of pGSN and pIgA induced glomerular fibrosis via the TGF-β1/Smads signal transduction pathway. This might be a potential mechanism for the glomerular fibrosis observed in IgAN patients.

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“…In human colon cancer cells, the overexpression of GSN was accompanied by the promotion of migration capacity. In addition, the decreased expression of GSN decreased the migratory potential of melanoma cells (30,(36)(37)(38)(39)(40). Therefore, GSN overexpression may result in positive effects that promote invasion and metastasis in oral cancer progression.…”

Section: Discussionmentioning

confidence: 99%

“…The current study indicated that the upregulation of GSN increased Tca8113 cell migration and invasion in vitro, which caused enhanced motility. In addition, it has been indicated that GSN may affect motility in human colon cancer and melanoma cells (30,(36)(37)(38)(39)(40). In human colon cancer cells, the overexpression of GSN was accompanied by the promotion of migration capacity.…”

Section: Discussionmentioning

confidence: 99%

Gelsolin regulates proliferation, apoptosis, migration and invasion in human oral carcinoma cells

et al. 2015

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Abstract. Gelsolin (GSN) is one of the most abundant actin-binding proteins, and is involved in several pathological processes, including Alzheimer's disease, cardiac injury and cancer. The aim of the present study was to assess the effect of GSN on the growth and motility of oral squamous cell carcinoma Tca8113 cells. The overexpression vector pcDNA3.1-GSN was transfected into Tca8113 cells and the stable GSN overexpression cell line was identified based on G418 antibiotic selection. The effect of GSN overexpression on the proliferation, apoptosis, migration and invasion of Tca8113 cells was examined using a cell counting kit-8 assay, flow cytometry and Transwell assays. The results revealed that GSN overexpression significantly promoted the cell proliferation and apoptosis of Tca8113 cells. In addition, Transwell assays demonstrated that the migration and invasion abilities of Tca8113 cells were enhanced by GSN overexpression. Therefore, the upregulation of GSN promotes cell growth and motility, indicating that it may perform a vital function in the progression of human oral cancers. IntroductionIn eukaryotic species, the actin cytoskeleton is essential for numerous cellular functions, including maintenance of morphology, motility, division, adhesion, endocytosis, intracellular transport and signal transduction (1-5). The varied and complex activities of the actin cytoskeleton are dynamically regulated by actin-binding proteins (ABPs) (2-4,6,7). Gelsolin (GSN) is one of the most abundant ABPs, and has been found to be a multifunctional regulator of physiological and pathological cellular processes (7,8).Previous studies have indicated that GSN may be a tumor suppressor that exerts a crucial role in the carcinogenic process (7,9). However, biphasic expression of GSN in oral precancerous lesions and oral cancers has been observed, which revealed a downregulation in GSN between oral precancerous lesions and oral cancers, and demonstrated upregulation of GSN in the stages of oral cancer progression (8). The biphasic expression indicated that GSN may perform a more complicated role in oral cancer biology.In order to study the biological roles in oral cancer development in the present study, GSN was overexpressed in oral cancer Tca8113 cells, and the effect of GSN on the proliferation, apoptosis, cell cycle, migration and invasion of these cells was investigated, which may contribute to the present understanding of the biological actions of GSN. Materials and methodsTca8113 cell culture. The human oral squamous cell carcinoma Tca8113 cell line was provided by the Shanghai Ninth People's Hospital, Medical School of Shanghai Jiao Tong University (Shanghai, China). The cells were cultured in RPMI 1640 medium (Gibco-BRL, Carlsbad, CA, USA) containing 10% fetal bovine serum (FBS), 100 µg/ml streptomycin and 100 units/ml penicillin, at 37˚C in a 5% CO 2 atmosphere.Stable transfection. To transiently transfect GSN into the Tca8113 cells, 0.5x10 5 cells/well were seeded into a 24-well plate (Corning, Inc., Corning, NY, USA)...

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Gelsolin affects the migratory ability of human colon adenocarcinoma and melanoma cells

Cited by 29 publications

References 37 publications

Overexpression of lumican affects the migration of human colon cancer cells through up-regulation of gelsolin and filamentous actin reorganization

Overexpression of lumican affects the migration of human colon cancer cells through up-regulation of gelsolin and filamentous actin reorganization

Plasma Gelsolin Induced Glomerular Fibrosis via the TGF-β1/Smads Signal Transduction Pathway in IgA Nephropathy

Gelsolin regulates proliferation, apoptosis, migration and invasion in human oral carcinoma cells

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