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. 2016 Jul 20;7(33):53254–53268. doi: 10.18632/oncotarget.10736

Figure 7. Schematic model depicting mediation of response to cisplatin-based primary chemotherapy by miR-770-5p and ERCC2 OVC patients.

Figure 7

(A) The general mechanism of ERCC2-dependent DNA damage repair after cisplatin treatment in OVC patients. After the DNA intra-strand is unwound and damaged by cisplatin, ERCC2 recognizes and repairs the DNA adducts. In OVC patients with IR to cisplatin, miR-770-5p is downregulated and does not suppress ERCC2 expression; ERCC2 is thus overexpressed in OVC cells and activates excision repair of DNA damaged by cisplatin, ultimately accelerating tumor cell growth (B) Conversely, in OVC patients with CR to cisplatin, miR-770-5p is upregulated and strongly suppresses ERCC2 expression in tumor cells; this reduces ERCC2-induced DNA damage repair, allowing cisplatin to damage DNA and ultimately activating tumor cell apoptosis (C) ERCC2 = excision repair cross-complementing rodent repair deficiency, group 2; IR = incomplete response; CR = complete response.