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2017 ; 13
(6
): 4147-4154
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Autophagy inhibition impairs the epithelial-mesenchymal transition and enhances
cisplatin sensitivity in nasopharyngeal carcinoma
#MMPMID28599416
Su Z
; Li G
; Liu C
; Ren S
; Deng T
; Zhang S
; Tian Y
; Liu Y
; Qiu Y
Oncol Lett
2017[Jun]; 13
(6
): 4147-4154
PMID28599416
show ga
Drug resistance restricts the efficacy of cisplatin in the treatment of
nasopharyngeal carcinoma (NPC). Increasing evidence indicates that autophagy and
the epithelial-mesenchymal transition (EMT) participate in cancer progression and
drug sensitivity. The aim of the present study was to investigate the function of
autophagy and EMT in cisplatin treatment, and to reveal the underlying impact of
autophagy on the EMT process in NPC. Transmission electron microscopy assays and
western blot analyses confirmed that cisplatin activates autophagy in NPC cells.
Alterations in cell morphology and biomolecular markers confirmed that cisplatin
induces the EMT phenotype in NPC cells. Cell viability assays showed that the
combination of the autophagy inhibitor chloroquine (CQ) increased the
cytotoxicity of cisplatin in NPC cells and that the EMT inducer transforming
growth factor ?1 promoted the resistance to cisplatin in NPC cells. Moreover,
autophagy inhibition by CQ and microtubule-associated protein 1 light chain
3B-knockdown reversed the EMT phenotype in NPC cells. In conclusion, autophagy
and the EMT process promote cisplatin resistance in NPC cells, while the
inhibition of autophagy impairs the EMT process.