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Antitumour effect of cyclin-dependent kinase inhibitors (p16(INK4A), p18(INK4C), p19(INK4D), p21(WAF1/CIP1) and p27(KIP1)) on malignant glioma cells.

Komata T, Kanzawa T, Takeuchi H, Germano IM, Schreiber M, Kondo Y, Kondo S - Br. J. Cancer (2003)

Bottom Line: It has not yet been fully determined, however, which CDKI is the best candidate for the treatment of malignant gliomas and whether normal brain tissues are affected by CDKI expression.On the other hand, p27(KIP1) overexpression did not inhibit the viability of cultured astrocytes (RNB) nor induced autophagy.Overall, our findings suggest that gene transfer of p27(KIP1) may be a promising approach for the therapy of malignant gliomas.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, Mount Sinai School of Medicine, New York, NY 10029, USA.

ABSTRACT
Cyclin-dependent kinase inhibitors (CDKIs) are considered as novel anticancer agents because of their ability to induce growth arrest or apoptosis in tumour cells. It has not yet been fully determined, however, which CDKI is the best candidate for the treatment of malignant gliomas and whether normal brain tissues are affected by CDKI expression. Using recombinant adenoviral vectors that express CDKIs (p16(INK4A), p18(INK4C), p19(INK4D), p21(WAF1/CIP1) and p27(KIP1)), we compared the antitumour effect of CDKIs on malignant glioma cell lines (A172, GB-1, T98G, U87-MG, U251-MG and U373-MG). p27(KIP1) showed higher ability to suppress the growth of all tumour cells tested than other CDKIs. Interestingly, overexpression of p27(KIP1) induced autophagic cell death, but not apoptosis in tumour cells. On the other hand, p27(KIP1) overexpression did not inhibit the viability of cultured astrocytes (RNB) nor induced autophagy. Overall, our findings suggest that gene transfer of p27(KIP1) may be a promising approach for the therapy of malignant gliomas.

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Related in: MedlinePlus

Effect of adenovirus expressing CDKIs on cell viability of malignant glioma cell lines. Tumour cells were seeded at 5 × 103 cells well−1 (0.1 ml) in 96-well flat-bottomed plates and incubated overnight at 37°C. On the following day, U373-MG, U251-MG, U87-MG cells, A172 cells, GB-1 and T98G cells were infected with AdBHGΔl,3, AdMH4pl6, AdMH4pl8, AdMH4pl9, AdMH4p21 or AdMH4p27 as indicated (day 0). On day 3, the cell viability was determined using a trypan blue dye exclusion assay. Values are given as the percentage of viable cells of AdBHGΔl ,3-infected cultures. Results shown are the means±s.d. of three independent experiments. U373-MG, U251-MG, U87-MG, A172 and GB-1 cells were infected at 60 MOI, while 180 MOI was used for T98G cells.
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fig1: Effect of adenovirus expressing CDKIs on cell viability of malignant glioma cell lines. Tumour cells were seeded at 5 × 103 cells well−1 (0.1 ml) in 96-well flat-bottomed plates and incubated overnight at 37°C. On the following day, U373-MG, U251-MG, U87-MG cells, A172 cells, GB-1 and T98G cells were infected with AdBHGΔl,3, AdMH4pl6, AdMH4pl8, AdMH4pl9, AdMH4p21 or AdMH4p27 as indicated (day 0). On day 3, the cell viability was determined using a trypan blue dye exclusion assay. Values are given as the percentage of viable cells of AdBHGΔl ,3-infected cultures. Results shown are the means±s.d. of three independent experiments. U373-MG, U251-MG, U87-MG, A172 and GB-1 cells were infected at 60 MOI, while 180 MOI was used for T98G cells.

Mentions: To investigate the effect of CDKI on malignant glioma cell lines, cell viability was determined 3 or 5 days after adenoviral infection. As shown in Figure 1Figure 1


Antitumour effect of cyclin-dependent kinase inhibitors (p16(INK4A), p18(INK4C), p19(INK4D), p21(WAF1/CIP1) and p27(KIP1)) on malignant glioma cells.

Komata T, Kanzawa T, Takeuchi H, Germano IM, Schreiber M, Kondo Y, Kondo S - Br. J. Cancer (2003)

Effect of adenovirus expressing CDKIs on cell viability of malignant glioma cell lines. Tumour cells were seeded at 5 × 103 cells well−1 (0.1 ml) in 96-well flat-bottomed plates and incubated overnight at 37°C. On the following day, U373-MG, U251-MG, U87-MG cells, A172 cells, GB-1 and T98G cells were infected with AdBHGΔl,3, AdMH4pl6, AdMH4pl8, AdMH4pl9, AdMH4p21 or AdMH4p27 as indicated (day 0). On day 3, the cell viability was determined using a trypan blue dye exclusion assay. Values are given as the percentage of viable cells of AdBHGΔl ,3-infected cultures. Results shown are the means±s.d. of three independent experiments. U373-MG, U251-MG, U87-MG, A172 and GB-1 cells were infected at 60 MOI, while 180 MOI was used for T98G cells.
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Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2747579&req=5

fig1: Effect of adenovirus expressing CDKIs on cell viability of malignant glioma cell lines. Tumour cells were seeded at 5 × 103 cells well−1 (0.1 ml) in 96-well flat-bottomed plates and incubated overnight at 37°C. On the following day, U373-MG, U251-MG, U87-MG cells, A172 cells, GB-1 and T98G cells were infected with AdBHGΔl,3, AdMH4pl6, AdMH4pl8, AdMH4pl9, AdMH4p21 or AdMH4p27 as indicated (day 0). On day 3, the cell viability was determined using a trypan blue dye exclusion assay. Values are given as the percentage of viable cells of AdBHGΔl ,3-infected cultures. Results shown are the means±s.d. of three independent experiments. U373-MG, U251-MG, U87-MG, A172 and GB-1 cells were infected at 60 MOI, while 180 MOI was used for T98G cells.
Mentions: To investigate the effect of CDKI on malignant glioma cell lines, cell viability was determined 3 or 5 days after adenoviral infection. As shown in Figure 1Figure 1

Bottom Line: It has not yet been fully determined, however, which CDKI is the best candidate for the treatment of malignant gliomas and whether normal brain tissues are affected by CDKI expression.On the other hand, p27(KIP1) overexpression did not inhibit the viability of cultured astrocytes (RNB) nor induced autophagy.Overall, our findings suggest that gene transfer of p27(KIP1) may be a promising approach for the therapy of malignant gliomas.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, Mount Sinai School of Medicine, New York, NY 10029, USA.

ABSTRACT
Cyclin-dependent kinase inhibitors (CDKIs) are considered as novel anticancer agents because of their ability to induce growth arrest or apoptosis in tumour cells. It has not yet been fully determined, however, which CDKI is the best candidate for the treatment of malignant gliomas and whether normal brain tissues are affected by CDKI expression. Using recombinant adenoviral vectors that express CDKIs (p16(INK4A), p18(INK4C), p19(INK4D), p21(WAF1/CIP1) and p27(KIP1)), we compared the antitumour effect of CDKIs on malignant glioma cell lines (A172, GB-1, T98G, U87-MG, U251-MG and U373-MG). p27(KIP1) showed higher ability to suppress the growth of all tumour cells tested than other CDKIs. Interestingly, overexpression of p27(KIP1) induced autophagic cell death, but not apoptosis in tumour cells. On the other hand, p27(KIP1) overexpression did not inhibit the viability of cultured astrocytes (RNB) nor induced autophagy. Overall, our findings suggest that gene transfer of p27(KIP1) may be a promising approach for the therapy of malignant gliomas.

Show MeSH
Related in: MedlinePlus