Characterization of the activities of actin-affecting drugs on tumor cell migration

Hayot, Caroline; Debeir, Olivier; Ham, Philippe Van; Damme, Marc Van; Kiss, Róbert; Decaestecker, Christine

doi:10.1016/j.taap.2005.06.006

Cited by 137 publications

(133 citation statements)

References 41 publications

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“…For isolation of Na 2 CO 3 -treated DRM (32) RBC membrane, 80% sucrose contained 0.3 M Na 2 CO 3 . For isolation of DRM after latrunculin A treatment (33,34), RBC were incubated with 1 M latrunculin A (Sigma) in PBS/glucose buffer at 37°C for 1 h. After incubation cells were washed and DRMs were obtained from RBC ghosts as described above.…”

Section: Methodsmentioning

confidence: 99%

Palmitoylation of MPP1 (Membrane-palmitoylated Protein 1)/p55 Is Crucial for Lateral Membrane Organization in Erythroid Cells

Lach

Grzybek

Heger

et al. 2012

Journal of Biological Chemistry

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Section: Methodsmentioning

confidence: 99%

Palmitoylation of MPP1 (Membrane-palmitoylated Protein 1)/p55 Is Crucial for Lateral Membrane Organization in Erythroid Cells

Lach

Grzybek

Heger

et al. 2012

Journal of Biological Chemistry

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“…Cancer progression involves a complex interplay between the tumor and the microenvironment that results in sustained proliferative signaling, resistance to cell death, as well as the promotion of angiogenesis, invasion, and metastasis (20)(21)(22)(23). This work has shown that ICOS binding to B7h influences several of these events by acting on both ECs and tumor cells.…”

Section: Discussionmentioning

confidence: 97%

B7h Triggering Inhibits the Migration of Tumor Cell Lines

Dianzani

Minelli

Gigliotti

et al. 2014

The Journal of Immunology

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Vascular endothelial cells (ECs) and several cancer cells express B7h, which is the ligand of the ICOS T cell costimulatory molecule. We have previously shown that B7h triggering via a soluble form of ICOS (ICOS-Fc) inhibits the adhesion of polymorphonuclear and tumor cell lines to HUVECs; thus, we suggested that ICOS-Fc may act as an anti-inflammatory and antitumor agent. Because cancer cell migration and angiogenesis are crucial for metastasis dissemination, the aim of this work was to evaluate the effect of ICOS-Fc on the migration of cancer cells and ECs. ICOS-Fc specifically inhibited the migration of HUVECs, human dermal lymphatic ECs, and the HT29, HCT116, PC-3, HepG2, JR8, and M14 tumor cell lines expressing high levels of B7h, whereas it was ineffective in the RPMI7932, PCF-2, LM, and BHT-101 cell lines expressing low levels of B7h. Furthermore, ICOS-Fc downmodulated hepatocyte growth factor facilitated the epithelial-to-mesenchymal transition in HepG2 cells. Moreover, ICOS-Fc downmodulated the phosphorylation of focal adhesion kinase and the expression of β-Pix in both HUVECs and tumor cell lines. Finally, treatment with ICOS-Fc inhibited the development of lung metastases upon injection of NOD-SCID-IL2Rγnull mice with CF-PAC1 cells, as well as C57BL/6 mice with B16-F10 cells. Therefore, the B7h−ICOS interaction may modulate the spread of cancer metastases, which suggests the novel use of ICOS-Fc as an immunomodulatory drug. However, in the B16-F10–metastasized lungs, ICOS-Fc also increased IL-17A/RORc and decreased IL-10/Foxp3 expression, which indicates that it also exerts positive effects on the antitumor immune response.

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“…Other antiactin (cytochalasin D, latrunculin A, and jasplakinolide) and antimicrotubule (taxol, taxotere, vincristine) drugs have similar abilities to block migration of cancer cells. 15 The pharmacological actin depolymerization agent Cytochalasin D (CytoD) also caused reorganization of the actin cytoskele- ton, as well as, increased synthesis and activation of MMP-2. These activities required a MAPK-dependent signaling pathway as studied in endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Cucurbitacin B markedly inhibits growth and rapidly affects the cytoskeleton in glioblastoma multiforme

Ding

Wakimoto

Xing

et al. 2008

Intl Journal of Cancer

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Glioblastoma Multiforme (GBM) is almost inevitably a fatal tumor of the brain with most individuals dying within 1 year of diagnosis. It is the most frequent brain tumor in adults. Dose-response studies showed that Cucurbitacin B inhibited 50% growth (ED 50 ) of 5 human GBM cell lines in liquid culture at 10 27 M. Soft-gel assays demonstrated that nearly all of the GBM clonogenic cells were inhibited at 10 28 M of Cucurbitacin B. FACS analysis found that the compound (10 27 M, 24 hr) caused G2/M arrest. The GBM cells underwent profound morphologic changes within 15-30 min after exposure to Cucurbitacin B (10 27 M), rounding up and losing their pseudopodia associated with disruption of actin and microtubules, as observed by immunoflourescence. Cucurbitacin B (10 27 M) caused prominent multinucleation of the cells after they were pulse-exposed (48 hr) to the drug, washed and cultured in normal medium for an additional 2 days. The drug (10 27 M, 3-24 hr) increased levels of p-p38, p-JNK and p-JUN in U87 and T98G GBM cell lines as seen by Western blot. Interestingly, alterations in cell morphology caused by Cucurbitacin B (10 27 M) were blocked by the JNK inhibitor SP600125. In summary, Cucurbitacin B has a prominent anti-proliferative activity on GBM cells; and at least in part, the mode of action is by affecting the cytoskeleton, as well as, the JNK pathway. Clinical trails of this drug should be pursued in GBM.

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Characterization of the activities of actin-affecting drugs on tumor cell migration

Cited by 137 publications

References 41 publications

Palmitoylation of MPP1 (Membrane-palmitoylated Protein 1)/p55 Is Crucial for Lateral Membrane Organization in Erythroid Cells

Palmitoylation of MPP1 (Membrane-palmitoylated Protein 1)/p55 Is Crucial for Lateral Membrane Organization in Erythroid Cells

B7h Triggering Inhibits the Migration of Tumor Cell Lines

Cucurbitacin B markedly inhibits growth and rapidly affects the cytoskeleton in glioblastoma multiforme

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