“…AKRs are stress response genes that promote resistance to cancer chemotherapeutic agents by protecting cancer cells from DNA damage. 30 , 31 , 32 , 33 Therefore, we speculate that SNORD60 may inhibit DSB repair in HB cells by downregulating AKR proteins. The mRNA level of AKR1C1/2 was not affected by SNORD60 overexpression ( Figure 6 M–N ).…”