Focus on ADF/Cofilin: Beyond Actin Cytoskeletal Regulation

Tsai, Cheng-Han; Lee, Yi Jang

doi:10.5402/2012/597876

Cited by 4 publications

(3 citation statements)

References 95 publications

(116 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cofilin 1 promoted proliferation and decreased apoptosis in T24 and RT4 cells. Furthermore, Cofilin 1 overexpression promoted cell cycle progression, while Cofilin 1 knockdown resulted in G1 phase arrest, which confirmed that Cofilin 1 promoted cell proliferation; however, this result contradicts previous results regarding the effects of Cofilin 1 on the cell cycle [ 33 , 34 ]. Cofilin 1 enhanced the migration and invasion capacities of T24 and RT4 cells, indicating that Cofilin 1 contributes to invasion and metastasis in bladder tumors as well as in mammary tumors [ 13 , 17 , 35 ].…”

Section: Discussioncontrasting

confidence: 56%

Cofilin 1 promotes bladder cancer and is regulated by TCF7L2

Wang

et al. 2017

Oncotarget

View full text Add to dashboard Cite

Earlier reports demonstrated that Cofilin expression is increased in bladder cancer samples, though its function remains unknown. Here, we found that Cofilin 1 expression was higher in bladder cancer tissues than in paracancerous tissues. Overexpression of Cofilin 1 promoted, while Cofilin 1 knockdown inhibited, proliferation, migration, and invasion in the T24 and RT4 bladder cancer cell lines. In addition, Cofilin 1 overexpression increased, while Cofilin 1 knockdown decreased, bladder tumor volumes in mouse xenograft experiments. Transcription factor 7-like 2 (TCF7L2) targeted the promoter of the Cofilin 1 gene, and TCF7L2 knockdown or mutations in the Cofilin 1 promoter dramatically decreased Cofilin 1 transcription. TCF7L2 promoted cell proliferation and migration and increased Cofilin 1 protein levels in RT4 and T24 cells. Thus, TCF7L2 contributed to Cofilin 1-induced promotion of bladder cancer development by binding to the Cofilin 1 promoter and increasing its expression.

show abstract

Section: Discussioncontrasting

confidence: 56%

Cofilin 1 promotes bladder cancer and is regulated by TCF7L2

Wang

et al. 2017

Oncotarget

View full text Add to dashboard Cite

show abstract

“…It was also revealed that DSGOST inhibits RhoA-mediated pathways for the phosphorylation of cofilin and MLC in coldand ET-1-exposed vascular cells, indicating that DSGOST may suppress contraction of vascular cells via regulation of actin reorganization (30)(31)(32)(33). Based on DSGOST inhibition of either RhoA activation or cytoskeletal reorganization, it is hypothesized that DSGOST may be useful in the management of other diseases with dysregulation of actin cytoskeleton in vascular cells.…”

Section: Discussionmentioning

confidence: 99%

Danggui-Sayuk-Ga-Osuyu-Senggang-Tang ameliorates cold-induced vasoconstriction in vitro and in vivo

Lee

Cho

Woo

et al. 2016

Molecular Medicine Reports

View full text Add to dashboard Cite

Danggui-Sayuk-Ga-Osuyu-Senggang-Tang (DSGOST), one of the traditional Chinese medicines, has long been prescribed for patients suffering from Raynaud phenomenon (RP) in Northeast Asian countries, including China, Japan and Korea. Although a previous in vitro study from our laboratory revealed that DSGOST prevents cold (25˚C)‑induced RhoA activation and endothelin‑1 (ET‑1) production in endothelial cells (ECs), the mechanisms by which DSGOST is able to alleviate the symptoms of RP have yet to be fully elucidated. The present study aimed to demonstrate that DSGOST regulates RhoA‑mediated pathways in cold‑exposed pericytes. In pericytes, DSGOST amplified cold‑induced RhoA activation, while markedly reducing ET‑1‑induced RhoA activation. Additionally, DSGOST‑mediated regulation of RhoA was closely associated with Rho‑associated, coiled‑coil‑containing protein kinase 1 (ROCK1)/testis‑specific kinase 1 (TESK1)/PDXP, but not with LIM domain kinase 1/2 (LIMK1/2), cofilin and myosin light chain (MLC). Thus, DSGOST activation of RhoA/ROCK1/TESK1/PDXP in cold‑exposed pericytes appeared to be crucial for treating vessel contraction. In addition, the DSGOST effect on the RhoA‑mediated pathway in cold‑induced human umbilical vein endothelial cells or human dermal microvascular endothelial cells was similar to that in ET‑1‑treated pericytes, but not in cold‑induced pericytes. The results of the present study further confirmed that DSGOST inhibits cold‑induced contraction of the mouse tail vein in vivo. Furthermore, DSGOST treatment reduced cold‑induced expression of the α2c‑adrenergic receptor in mouse tail vessels. Therefore, the data in the present study suggest that DSGOST may be useful for the treatment of RP‑like disease.

show abstract

“…These sustain the balance of actin polymerization and depolymerization and therefore are strongly controlled in their expression and activity pattern [ 16 ],[ 18 ],[ 21 ]. Here, the actin regulatory protein, actin depolymerization factor (ADF)/cofilin acts as a key player by severing filaments [ 22 ]. ADF/cofilin becomes inactive when it is phosphorylated at its serine 3 residue.…”

Section: Introductionmentioning

confidence: 99%

Membrane related dynamics and the formation of actin in cells growing on micro-topographies: a spatial computational model

et al. 2014

View full text Add to dashboard Cite

BackgroundIntra-cellular processes of cells at the interface to an implant surface are influenced significantly by their extra-cellular surrounding. Specifically, when growing osteoblasts on titanium surfaces with regular micro-ranged geometry, filaments are shorter, less aligned and they concentrate at the top of the geometric structures. Changes to the cytoskeleton network, i. e., its localization, alignment, orientation, and lengths of the filaments, as well as the overall concentration and distribution of key-actors are induced. For example, integrin is distributed homogeneously, whereas integrin in activated state and vinculin, both components of focal adhesions, have been found clustered on the micro-ranged geometries. Also, the concentration of Rho, an intracellular signaling protein related to focal adhesion regulation, was significantly lower.ResultsTo explore whether regulations associated with the focal adhesion complex can be responsible for the changed actin filament patterns, a spatial computational model has been developed using ML-Space, a rule-based model description language, and its associated Brownian-motion-based simulator. The focus has been on the deactivation of cofilin in the vicinity of the focal adhesion complex. The results underline the importance of sensing mechanisms to support a clustering of actin filament nucleations on the micro-ranged geometries, and of intracellular diffusion processes, which lead to spatially heterogeneous distributions of active (dephosphorylated) cofilin, which in turn influences the organization of the actin network. We find, for example, that the spatial heterogeneity of key molecular actors can explain the difference in filament lengths in cells on different micro-geometries partly, but to explain the full extent, further model assumptions need to be added and experimentally validated. In particular, our findings and hypothesis referring to the role, distribution, and amount of active cofilin have still to be verified in wet-lab experiments.ConclusionLetting cells grow on surface structures is a possibility to shed new light on the intricate mechanisms that relate membrane and actin related dynamics in the cell. Our results demonstrate the need for declarative expressive spatial modeling approaches that allow probing different hypotheses, and the central role of the focal adhesion complex not only for nucleating actin filaments, but also for regulating possible severing agents locally.

show abstract

Focus on ADF/Cofilin: Beyond Actin Cytoskeletal Regulation

Cited by 4 publications

References 95 publications

Cofilin 1 promotes bladder cancer and is regulated by TCF7L2

Cofilin 1 promotes bladder cancer and is regulated by TCF7L2

Danggui-Sayuk-Ga-Osuyu-Senggang-Tang ameliorates cold-induced vasoconstriction in vitro and in vivo

Membrane related dynamics and the formation of actin in cells growing on micro-topographies: a spatial computational model

Contact Info

Product

Resources

About