Wang X(1), Chen B(1)(2)(3), Xu D(1), Li Z(4), Liu H(4), Huang Z(1)(2)(3), Huang K(4), Lin X(1)(2)(3), Yao H(1)(2)(3). Author information:
(1)Department of Pharmaceutical Analysis, School of Pharmacy, Fujian Medical
University, Fuzhou, Fujian, China.
(2)Nano Medical Technology Research Institute, Fujian Medical University,
Fuzhou, Fujian, China.
(3)Higher Educational Key Laboratory for Nano Biomedical Technology of Fujian
Province, Fujian Medical University, Fuzhou, Fujian, China.
(4)School of Pharmacy, Fujian Medical University, Fuzhou, Fujian, China.
Here, we review the molecular mechanism and pharmacokinetics of flavonoids in the treatment of resistant EGF receptor (EGFR)-mutated non-small-cell lung cancer (NSCLC) and particularly the possible mechanism(s) of delicaflavone, a biflavonoid extracted from Selaginella doederleinii Hieron. EGFR TK inhibitors (EGFR-TKI) are ubiquitously used in the treatment of NSCLC bearing EGFR mutations. However, patients treated with EGFR-TKI inevitably and continuously develop resistance. In laboratory studies, flavonoids, as potential adjuvants for cancer chemotherapy, exhibited anti-cancer properties such as inhibition of chemoresistance by interference with ABC transporters-induced drug efflux, curbing of c-MET amplification, or reversal of T790M mutation-mediated resistance. The current review aims at summarizing the association between the anti-cancer potentials of flavonoids and their possible regulatory roles in certain types of mutation that could trigger EGFR-TKI resistance in NSCLC. Potential practical applications of these phytochemicals, as well as the relevant pharmacokinetics, are also discussed.
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