Indibulin, a Novel Microtubule Inhibitor, Discriminates between Mature Neuronal and Nonneuronal Tubulin

Wienecke, Anke; Bacher, Gerald

doi:10.1158/0008-5472.can-08-1342

Cited by 72 publications

(46 citation statements)

References 33 publications

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“…Treatment with nocodazole, which caused depolymerization of many of the microtubules (Figure 5), reversed the morphological changes induced in RR25 cells (Figure 1A, nocodazole). In addition, treatment with indibulin, a compound reported to only effect non-acetylated microtubules (Wienecke and Bacher 2009), also reversed the morphological transformation in RR25 cells (Figure 1A, indibulin). Interestingly, neither nocodazole nor indibulin had any effect on the transformation of the RIE cells over-expressing H-Ras V12 (Figure 1A).…”

Section: Resultsmentioning

confidence: 81%

Transformation of rat intestinal epithelial cells by overexpression of Rab25 is microtubule dependent

et al. 2011

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Little research has addressed the role of membrane trafficking and recycling in the regulation of the transformed phenotype of neoplastic cells. The small GTPase Rab25 is an epithelial-specific modulator of membrane recycling. Recent studies have demonstrated that Rab25 expression is up-regulated in a number of epithelial cancers and over-expression may increase the aggressive phenotype of certain cancers. We have utilized the non-transformed RIE cell line to examine the influence of Rab25 on transformation. Over-expression of Rab25 in RIE cells leads to morphological transformation as well as growth in soft agar, tumor formation in nude mice, disruption of integrin-based focal adhesions and alteration in modified microtubule subsets. Although the predominance of recent cancer research has focused on the manipulation of the actin-based cytoskeleton, recycling trafficking relies on microtubules. Transformation of RIE cells through over-expression of Rab25, but not with H-RasV12, was reversed by inhibitors of microtubule polymerization. These results suggest that up-regulation of Rab25 in RIE cells leads to microtubule-dependent transformation. Thus, depolymerization of microtubules may be a potent therapeutic target for cancer therapy through the reversal of the invasive phenotype of certain cancer cells.

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Section: Resultsmentioning

confidence: 81%

Transformation of rat intestinal epithelial cells by overexpression of Rab25 is microtubule dependent

et al. 2011

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“…NGF contributes to the neuronal survival by activating AKT following activating phosphoinositide 3-kinase (Yao and Cooper 1995;Dudek et al 1997). NGF regulation of microtubule may not be critical to survival of PC12 cells compared to proliferation and differentiation (Black et al 1986;Wienecke and Bacher 2009).…”

Section: Resultsmentioning

confidence: 99%

Colchicine-Induced Apoptosis Was Prevented by Glycogen Synthase Kinase-3 Inhibitors in PC12 Cells

2010

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The purpose of this study was to examine whether glycogen synthase kinase-3 (GSK-3) is involved in colchicine-induced cell death in PC12 cells by using GSK inhibitors. Colchicine increased apoptotic cell death with morphological changes characterized by cell shrinkage and nuclear condensation or fragmentation. GSK-3 inhibitors such as alsterpaullone, SB216763, and AR-A014418 prevented colchicine-induced cell death and caspase-3 activation. These results suggest that colchicine induces caspase-dependent apoptotic cell death and that GSK-3 activation is involved in cell death in PC12 cells.

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“…Because of its high toxicity, it is not used for cancer therapy. 92 Inhibitors of mitotic kinesin motors are a new type of antimitotic agents. 93,94 Kinesin spindle protein (Eg5/KSP), 95 a microtubule-associated motor protein essential for cell cycle progression and the proper partitioning of sister chromatids, is overexpressed in many cancer cells.…”

Section: Antimitotic Agentsmentioning

confidence: 99%

Natural Products from Terrestrial Microbial Organisms with Cytotoxic Cell Cycle Inhibitors

Dreis¹,

Gartner²,

Krebs³

et al. 2014

Biodiversity, Natural Products and Cancer Treatment

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Many microbial products have the potential for therapeutic application, e.g. as anticancer drugs. This chapter presents natural products from terrestrial microbial organisms that attack various targets in tumor cells, e.g. cell cycle inhibitors (inhibitors of phosphoinositide-3-kinase, checkpoint kinase inhibitors, inhibitors of dual specificity phosphatases, inhibitors of cyclin-dependent kinases), inhibitors of histone deacetylases, topoisomerases, or growth factors as well as inhibitors of the proteasome, of heat shock protein 90, nuclear trafficking, or ATPase.New cancer drugs are most likely be used as part of combination therapy regimens. Attacking different targets in tumor cells may kill tumor cells resistant to one target. The potential of novel target-directed compounds to eradicate otherwise drug-resistant cells is an attractive perspective, which deserves further investigation.

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Indibulin, a Novel Microtubule Inhibitor, Discriminates between Mature Neuronal and Nonneuronal Tubulin

Cited by 72 publications

References 33 publications

Transformation of rat intestinal epithelial cells by overexpression of Rab25 is microtubule dependent

Transformation of rat intestinal epithelial cells by overexpression of Rab25 is microtubule dependent

Colchicine-Induced Apoptosis Was Prevented by Glycogen Synthase Kinase-3 Inhibitors in PC12 Cells

Natural Products from Terrestrial Microbial Organisms with Cytotoxic Cell Cycle Inhibitors

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