Pub. Date : 2011 May
PMID : 21377995
6 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | N-methylpurine DNA glycosylase and DNA polymerase beta modulate BER inhibitor potentiation of glioma cells to temozolomide. | Temozolomide | N-methylpurine DNA glycosylase | Homo sapiens |
| 2 | N-methylpurine DNA glycosylase (MPG) initiates BER by removing TMZ-induced N3-methyladenine and N7-methylguanine base lesions, leaving abasic sites (AP sites) in DNA for further processing by BER. | Temozolomide | N-methylpurine DNA glycosylase | Homo sapiens |
| 3 | N-methylpurine DNA glycosylase (MPG) initiates BER by removing TMZ-induced N3-methyladenine and N7-methylguanine base lesions, leaving abasic sites (AP sites) in DNA for further processing by BER. | Temozolomide | N-methylpurine DNA glycosylase | Homo sapiens |
| 4 | Using the human glioma cell lines LN428 and T98G, we report here that potentiation of TMZ via BER inhibition [methoxyamine (MX), the PARP inhibitors PJ34 and ABT-888 or depletion (knockdown) of PARG] is greatly enhanced by over-expression of the BER initiating enzyme MPG. | Temozolomide | N-methylpurine DNA glycosylase | Homo sapiens |
| 5 | We also show that methoxyamine-induced potentiation of TMZ in MPG expressing glioma cells is abrogated by elevated-expression of the rate-limiting BER enzyme DNA polymerase beta (Polbeta), suggesting that cells proficient for BER readily repair AP sites in the presence of MX. | Temozolomide | N-methylpurine DNA glycosylase | Homo sapiens |
| 6 | This study demonstrates that MPG overexpression, together with inhibition of BER, sensitizes glioma cells to the alkylating agent TMZ in a Polbeta-dependent manner, suggesting that the expression level of both MPG and Polbeta might be used to predict the effectiveness of MX and PARP-mediated potentiation of TMZ in cancer treatment. | Temozolomide | N-methylpurine DNA glycosylase | Homo sapiens |