Title : p53 sensitizes chemoresistant non-small cell lung cancer via elevation of reactive oxygen species and suppression of EGFR/PI3K/AKT signaling.

Pub. Date : 2019

PMID : 31360122






7 Functional Relationships(s)
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Protein Name
Organism
1 Somatic mutation of TP53 (36%) and epidermal growth factor receptor (EGFR; > 30%) are major contributors to cisplatin (CDDP) resistance. Cisplatin epidermal growth factor receptor Homo sapiens
2 Somatic mutation of TP53 (36%) and epidermal growth factor receptor (EGFR; > 30%) are major contributors to cisplatin (CDDP) resistance. Cisplatin epidermal growth factor receptor Homo sapiens
3 Somatic mutation of TP53 (36%) and epidermal growth factor receptor (EGFR; > 30%) are major contributors to cisplatin (CDDP) resistance. Cisplatin epidermal growth factor receptor Homo sapiens
4 Somatic mutation of TP53 (36%) and epidermal growth factor receptor (EGFR; > 30%) are major contributors to cisplatin (CDDP) resistance. Cisplatin epidermal growth factor receptor Homo sapiens
5 Results: We have demonstrated for the first time that activation of p53 sensitizes chemoresistant NSCLC cells to CDDP by down-regulating EGFR signaling pathway and promoting intracellular ROS production. Cisplatin epidermal growth factor receptor Homo sapiens
6 Our findings suggest that CDDP-induced apoptosis in chemosensitive NSCLC cells involves p53 activation, leading to suppressed EGFR signaling and ROS production. Cisplatin epidermal growth factor receptor Homo sapiens
7 In contrast, in chemoresistant NSCLC, activated Akt promotes EGFR signaling by the positive feedback loop and suppresses CDDP-induced ROS production and apoptosis. Cisplatin epidermal growth factor receptor Homo sapiens