Suppression of the Invasive Capacity of Rat Ascites Hepatoma Cells by Knockdown of Slingshot or LIM Kinase

Horita, Yuji; Ohashi, Kazumasa; Mukai, Mutsuko; Inoue, Masahiro; Mizuno, Kensaku

doi:10.1074/jbc.m706538200

Cited by 51 publications

(24 citation statements)

References 48 publications

(68 reference statements)

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“…By contrast, in the invasive subpopulation of tumor cells in different types of mammary tumors, LIMK is spontaneously overexpressed together with either cofilin [MTLn3 tumors ] or the cofilin activator SSH [PyMT tumors (Wang et al, 2007b)]. Similar findings were obtained in other cell systems; for example, in rat ascites hepatoma (MM1) cells, the knockdown of SSH inhibits migration and invasion, and knockdown of LIMK has the same effect (Horita et al, 2008). The simultaneous overexpression of both the inhibitory and stimulatory components of the cofilin pathway sharpens the local activation of cofilin in these cells (LEGI model) and therefore increases the transient barbed-end output of the cofilin pathway in response to EGF (thereby increasing chemotaxis and motility) Wang et al, 2007b).…”

Section: Cofilin Activation In Mammary-tumor Cells Is Dependent On Plsupporting

confidence: 63%

A common cofilin activity cycle in invasive tumor cells and inflammatory cells

Rheenen

Condeelis

Glogauer

2009

Journal of Cell Science

109

119

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In many cell types, the formation of membrane protrusions and directional migration depend on the spatial and temporal regulation of the actin-binding protein cofilin. Cofilin, which is important for the regulation of actin-polymerization initiation, increases the number of actin free barbed ends through three mechanisms: its intrinsic actin-nucleation activity; binding and severing of existing actin filaments; and recycling actin monomers from old filaments to new ones through its actin-depolymerization activity. The increase in free barbed ends that is caused by cofilin initiates new actin polymerization, which can be amplified by the actin-nucleating ARP2/3 complex. Interestingly, different cell systems seem to have different mechanisms of activating cofilin. The initial activation of cofilin in mammary breast tumors is dependent on PLCγ, whereas cofilin activation in neutrophils is additionally dependent on dephosphorylation, which is promoted through Rac2 signaling. Although the literature seems to be confusing and inconsistent, we propose that all of the data can be explained by a single activity-cycle model. In this Opinion, we give an overview of cofilin activation in both tumor cells and inflammatory cells, and demonstrate how the differences in cofilin activation that are observed in various cell types can be explained by different starting points in this single common activity cycle.

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Section: Cofilin Activation In Mammary-tumor Cells Is Dependent On Plsupporting

confidence: 63%

A common cofilin activity cycle in invasive tumor cells and inflammatory cells

Rheenen

Condeelis

Glogauer

2009

Journal of Cell Science

109

119

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“…LIMKs also translocate from the cortical cytoplasm and focal adhesions, where they modulate cell morphology and motility, and to the centrosome and nucleus, where they regulate mitosis and cytokinesis (34). LIMKs are overexpressed and implicated in various cancers, such as breast, lung, skin, liver and prostate, and several tumor cell lines (35, 36). Down-regulation of LIMK1 activity reduces the invasiveness in several cancer cells, such as breast cancer and hepatoma cells (37).…”

Section: Introductionmentioning

confidence: 99%

Molecular Pathways: Targeting the Kinase Effectors of RHO-Family GTPases

Prudnikova

Rawat

Chernoff

2015

Clinical Cancer Research

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RHO GTPases, members of the RAS superfamily of small GTPases, are adhesion and growth-factor activated molecular switches that play important roles in tumor development and progression. When activated, RHO-family GTPases such as RAC1, CDC42, and RHOA, transmit signals by recruiting a variety of effector proteins, including the protein kinases PAK, ACK, MLK, MRCK, and ROCK. Genetically-induced loss of RHO function impedes transformation by a number of oncogenic stimuli, leading to an interest in developing small molecule inhibitors that either target RHO GTPases directly, or that target their downstream protein kinase effectors. Although inhibitors of RHO GTPases and their downstream signaling kinases have not yet been widely adopted for clinical use, their potential value as cancer therapeutics continues to facilitate pharmaceutical research and development and is a promising therapeutic strategy.

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“…Small interfering RNAs (siRNAs) of LIMK1 were subcloned into the pSuper-EGFP vectors (OligoEngine, Seattle, WA). The target sequence for rat Limk1 genes was described previously (31,32), 5Ј-GAC-TTGCGTAGCCTTAAGA-3Ј (LIMK1 siRNA1) and 5Ј-GCT-GGAACAATGGCTAGAA-3Ј (LIMK1 siRNA2). All the constructs were confirmed by DNA sequencing.…”

Section: Methodsmentioning

confidence: 99%

LIM Kinase 1 (LIMK1) Interacts with Tropomyosin-related Kinase B (TrkB) and Mediates Brain-derived Neurotrophic Factor (BDNF)-induced Axonal Elongation

Dong

Cai

et al. 2012

Journal of Biological Chemistry

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Background: BDNF promotes axonal outgrowth, whereas the underlying molecular mechanism has remained unclear. Results: LIMK1 interacts with TrkB, and BDNF treatment could induce LIMK1 dimerization and transactivation, which facilitate axonal elongation. Conclusion: LIMK1-regulated actin dynamics is essential for BDNF-induced axonal elongation. Significance: These results revealed a novel mechanism for the BDNF-induced axonal elongation.

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Suppression of the Invasive Capacity of Rat Ascites Hepatoma Cells by Knockdown of Slingshot or LIM Kinase

Cited by 51 publications

References 48 publications

A common cofilin activity cycle in invasive tumor cells and inflammatory cells

A common cofilin activity cycle in invasive tumor cells and inflammatory cells

Molecular Pathways: Targeting the Kinase Effectors of RHO-Family GTPases

LIM Kinase 1 (LIMK1) Interacts with Tropomyosin-related Kinase B (TrkB) and Mediates Brain-derived Neurotrophic Factor (BDNF)-induced Axonal Elongation

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