| Summary: | Lung adenocarcinomas exhibit chemoresistance mostly due to deregulation of nuclear factor erythroid-derived 2-like 2 (Nrf2). Epigallocatechin gallate (EGCG), was investigated for altering Nrf2 mediated etoposide resistance in different lung adenocarcinoma cells. In A549, EGCG downregulated nuclear Nrf2 by upregulating the nuclear localization of Keap1 whereas in NCIH23, EGCG augmented Nrf2 by reducing Keap1. In Keap-1 independent mode EGCG increased p53, and decreased p21, in A549 but in NCIH23 vice versa was observed. EGCG enhanced retinoid X receptor (RXR) in both A549 and NCIH23 but retinoid acid receptor (RAR) was aggravated in A549 and suppressed in NCIH23. Though the direction of Nrf2 regulation was opposite in two cell lines, optimum level of Nrf2 was maintained which increased responsiveness towards etoposide. EGCG sensitized/potentiated lung adenocarcinoma cells towards chemotherapy by inducing G2/M arrest and suppressing the multi-drug resistance. Thus, EGCG might have a novel implication in chemotherapeutic management of lung cancer cells.
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