Autophagosome accumulation-mediated ATP energy deprivation induced by penfluridol triggers nonapoptotic cell death of lung cancer via activating unfolded protein response.

ABSTRACT: Anticancer chemotherapeutic drugs mainly trigger apoptosis induction to eliminate malignant cells. However, many cancer cells are chemoresistant because of defective apoptosis induction. Targeting the autophagic pathway is currently regarded as an alternative strategy for cancer drug discovery. Penfluridol, an antipsychotic drug, has been reported to exert oncostatic effects, but the effect of penfluridol on lung cancer remains unknown. Herein, the antitumor activity of penfluridol was determined in vitro in non-small-cell lung cancer (NSCLC) cell lines using MTS, plate clonogenic, and transwell migration assays and in vivo in an orthotopic xenograft model. Flow cytometry, holotomographic microscopy, immunofluorescence, and immunohistochemistry were employed to determine the cell-death phe

SUBMITTER: Hung WY 

PROVIDER: S-EPMC6629704 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature