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Figure 4 | Journal of Translational Medicine

Figure 4

From: miR-130a can predict response to temozolomide in patients with glioblastoma multiforme, independently of O6-methylguanine-DNA methyltransferase

Figure 4

Lower miR-130a could generate more extensive response to oxidative stress, which in turn could elevate Ape1 and the repair of abasic sites. In double-stranded DNA, N7-methylguanine (7-meG), N3-methyladenine (3-meA) and O6-methylguanine (O6-meG) accounts for approximately 70, 10, and 7% of temozolomide (TMZ)-induced DNA adducts, respectively. O6-meG adduct is repaired by O6-methylguanine-DNA methyltransferase (MGMT). 7-meG and 3-meA could generate abasic sites, which can impede DNA replication. Apurinic/apyrimidinic endonuclease 1 (Ape1) is the key enzyme that removes abasic sites. Patients with lower miR-130a could generate a more extensive response to oxidative stress, which in turn could elevate Ape1 and the repair of abasic sites, finally mediating resistance to TMZ.

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