Staurosporine-induced Growth Inhibition of Glioma Cells is Accompanied by Altered Expression of Cyclins, CDKs and CDK Inhibitors

Harmalkar, Mugdha; Shirsat, Neelam

doi:10.1007/s11064-006-9068-0

Cited by 15 publications

(7 citation statements)

References 20 publications

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“…Genes in this pathway were also suggested to be related with glioma. Take CDK2 for example, this gene was reported to be suppressed during the inhibition of glioma cells (Harmalkar and Shirsat, 2006). This is consistent with our results, since CDK2 is overexpressed in grade IV patients.…”

Section: Discussionsupporting

confidence: 91%

Pathway and Network Analysis in Glioma with the Partial Least Squares Method

Gu²,

Shou³

2014

Asian Pacific Journal of Cancer Prevention

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Section: Discussionsupporting

confidence: 91%

Pathway and Network Analysis in Glioma with the Partial Least Squares Method

Gu²,

Shou³

2014

Asian Pacific Journal of Cancer Prevention

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“…As a positive control, we used staurosporine (STS) a known inducer of apoptosis in human glioma cell lines, including U87. 27 zVAD inhibited STS-induced apoptosis by .25% (Fig. 4E).…”

Section: Lanatoside C Induces a Necrosis-like Caspase-independent Cell Deathmentioning

confidence: 86%

Lanatoside C sensitizes glioblastoma cells to tumor necrosis factor–related apoptosis-inducing ligand and induces an alternative cell death pathway

et al. 2011

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Human glioblastoma (GBM) cells are notorious for their resistance to apoptosis-inducing therapeutics. We have identified lanatoside C as a sensitizer of GBM cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced cell death partly by upregulation of the death receptor 5. We show that lanatoside C sensitizes GBM cells to TRAIL-induced apoptosis in a GBM xenograft model in vivo. Lanatoside C on its own serves as a therapeutic agent against GBM by activating a caspase-independent cell death pathway. Cells treated with lanatoside C showed necrotic cell morphology with absence of caspase activation, low mitochondrial membrane potential, and early intracellular ATP depletion. In conclusion, lanatoside C sensitizes GBM cells to TRAIL-induced cell death and mitigates apoptosis resistance of glioblastoma cells by inducing an alternative cell death pathway. To our knowledge, this is one of the first examples of use of caspase-independent cell death inducers to trigger tumor regression in vivo. Activation of such mechanism may be a useful strategy to counter resistance of cancer cells to apoptosis.

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“…Compound (2) showed significant CDK inhibition IC 50 (CDK2/cyclin A = 0.007 μM, [36] CDK4/cyclin D = 3-10 μM) [37]. The levels of CDK2, cdc2, cyclin A and cyclin B proteins decreased, while the levels of CDK inhibitors viz., p21 and p27 were found to increase on treatment with compound (2) [38]. The levels of CDK2, cdc2, cyclin A and cyclin B proteins decreased, while the levels of CDK inhibitors viz., p21 and p27 were found to increase on treatment with compound (2) [38].…”

Section: Staurosporine and Analoguesmentioning

confidence: 97%

“…The pyrido[2,3-d]pyrimidin-7-one template (38) had been identified as a privileged structure for the inhibition of ATPdependent kinase and good potency against CDKs had been reported for representative examples [111]. The introduction of the methyl substituent at the C-5 position of (38) confer excellent selectivity for CDK4 versus other CDKs and representative tyrosine kinases.…”

Section: Pyrimidines Derivativesmentioning

confidence: 99%

Inhibitors of Cyclin Dependent Kinases: Useful Targets for Cancer Treatment

Sharma¹,

Sharma²,

Tyagi³

2008

CCDT

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Cancer drug discovery is one of the most rapidly changing areas of pharmaceutical research. Uncontrolled proliferation is a hallmark of cancer cells. Over the past two decades, it has become increasingly clear that in many human cancers, hyperactivity of Cyclin Dependent Kinases (CDKs) is one of the mechanisms underlying the physiological hyper-proliferation. CDKs are serine/threonine protein kinases, which play an important role in cell-cycle regulation. Their sequential activation ensures, the correct timing and ordering of events required for cell cycle progression. Therefore, inhibition of CDKs, through the insertion of small molecules into its ATP binding pocket has emerged as a potential therapy method for cancers. Consequently, a number of small molecules with CDK inhibitory properties have been developed. Many of these have been evaluated as potent inhibitors and some are currently in clinical-trials for various types of cancer. This review reports various CDK inhibitors, natural as well as small molecules, along with their reported activities for various CDKs. It will highlight the potential for the development of novel anti-cancer molecules.

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Staurosporine-induced Growth Inhibition of Glioma Cells is Accompanied by Altered Expression of Cyclins, CDKs and CDK Inhibitors

Cited by 15 publications

References 20 publications

Pathway and Network Analysis in Glioma with the Partial Least Squares Method

Pathway and Network Analysis in Glioma with the Partial Least Squares Method

Lanatoside C sensitizes glioblastoma cells to tumor necrosis factor–related apoptosis-inducing ligand and induces an alternative cell death pathway

Inhibitors of Cyclin Dependent Kinases: Useful Targets for Cancer Treatment

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