Title : Identification of a novel mechanism for reversal of doxorubicin-induced chemotherapy resistance by TXNIP in triple-negative breast cancer via promoting reactive oxygen-mediated DNA damage.

Pub. Date : 2022 Apr 12

PMID : 35414060






3 Functional Relationships(s)
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1 In addition, we found that the small molecule c-Myc inhibitor 10058-F4 promoted TXNIP expression, increased ROS synthesis in cells, and could enhance the cytotoxicity of chemotherapy drugs in vitro and in vivo when combined with DOX. 5-(4-ethylbenzylidene)-2-thioxothiazolidin-4-one thioredoxin interacting protein Homo sapiens
2 These results indicated that c-Myc inhibitor 10058-F4 could induce TXNIP upregulation in TNBC drug-resistant cells, and the upregulated TXNIP increased the accumulation of ROS-dependent DNA damage, thereby decreasing chemotherapy resistance of TNBC. 5-(4-ethylbenzylidene)-2-thioxothiazolidin-4-one thioredoxin interacting protein Homo sapiens
3 These results indicated that c-Myc inhibitor 10058-F4 could induce TXNIP upregulation in TNBC drug-resistant cells, and the upregulated TXNIP increased the accumulation of ROS-dependent DNA damage, thereby decreasing chemotherapy resistance of TNBC. 5-(4-ethylbenzylidene)-2-thioxothiazolidin-4-one thioredoxin interacting protein Homo sapiens