Open AccessRepurposing antitussive benproperine phosphate against pancreatic cancer depends on autophagy arrest
Author(s) -
Zhang Huanyu,
Zhang Zhe,
Huang Yonghao,
Qin Siyuan,
Zhou Li,
Weng Ningna,
Liu Jiayang,
Yang Mei,
Zhang Xiaodian,
Lu Yanda,
Ma Lin,
Zheng Shaojiang,
Li Qifu
Publication year - 2021
Publication title -
molecular oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.332
H-Index - 88
eISSN - 1878-0261
pISSN - 1574-7891
DOI - 10.1002/1878-0261.12854
Subject(s) - autophagy , pi3k/akt/mtor pathway , pancreatic cancer , ampk , autophagosome , programmed cell death , in vivo , atg5 , microbiology and biotechnology , lysosome , cancer research , cancer cell , chemistry , pharmacology , biology , apoptosis , cancer , signal transduction , phosphorylation , biochemistry , protein kinase a , genetics , enzyme
Here, we show that benproperine phosphate (BPP), a cough suppressant, triggers AMPK/mTOR‐mediated autophagy initiation and disturbs Ras‐related protein Rab‐11A (RAB11A)‐mediated autophagosome–lysosome fusion, resulting in excessive accumulation of autophagosomes in pancreatic cancer (PC) cells. Inhibition of autophagy or overexpression of RAB11A partially reverses BPP‐induced growth inhibition in PC cells, suggesting BPP as a potent anti‐PC agent via the induction of autophagy arrest.