Open Access

Nifuroxazide induces the apoptosis of human non‑small cell lung cancer cells through the endoplasmic reticulum stress PERK signaling pathway

  • Authors:
    • Deliang Li
    • Liping Liu
    • Feng Li
    • Chengshan Ma
    • Keli Ge
  • View Affiliations

  • Published online on: April 25, 2023     https://doi.org/10.3892/ol.2023.13834
  • Article Number: 248
  • Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The aim of the present study was to investigate the molecular mechanism of nifuroxazide (NFZ) in the induction of apoptosis of NCI‑H1299 human non‑small cell lung cancer (NSCLC) cells through the reactive oxygen species (ROS)/Ca2+/protein kinase R‑like ER kinase (PERK)-activating transcription factor 4 (ATF4)‑DNA damage inducible transcript 3 (CHOP) signaling pathway. Morphological changes of cells were observed by microscopy, and the apoptosis and intracellular ROS levels of cells were observed by inverted fluorescence microscopy. Cell viability after the addition of the PERK inhibitor, GSK2606414, were detected by Cell Counting Kit‑8 assay. Annexin V‑FITC was used to detect cell apoptosis, Brite 670 was used to detect intracellular ROS and Fura Red AM was used to detect Ca2+ content. Western blotting was used to detect PERK, phosphorylated (P)‑PERK, ATF4, CHOP, P‑Janus kinase 2 and P‑signal transducer and activator of transcription 3 expression levels. Compared with the dimethyl sulfoxide control group, NFZ inhibited the survival activity in the H1299 NSCLC cell line, in a time‑ and dose‑dependent manner. However, GSK2606414 inhibited the NFZ‑induced apoptosis of H1299 cells. GSK2606414 also inhibited the increase in ROS and Ca2+ in H1299 cells induced by NFZ. Western blotting results demonstrated that NFZ significantly increased the expression levels of P‑PERK, ATF4 and CHOP, whereas GSK2606414 significantly reduced the NFZ‑induced increase in these protein expression levels. In conclusion, NFZ may induce the apoptosis of H1299 NSCLC cells through the ROS/Ca2+/PERK‑ATF4‑CHOP signaling pathway.
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June-2023
Volume 25 Issue 6

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Copy and paste a formatted citation
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Spandidos Publications style
Li D, Liu L, Li F, Ma C and Ge K: Nifuroxazide induces the apoptosis of human non‑small cell lung cancer cells through the endoplasmic reticulum stress PERK signaling pathway. Oncol Lett 25: 248, 2023
APA
Li, D., Liu, L., Li, F., Ma, C., & Ge, K. (2023). Nifuroxazide induces the apoptosis of human non‑small cell lung cancer cells through the endoplasmic reticulum stress PERK signaling pathway. Oncology Letters, 25, 248. https://doi.org/10.3892/ol.2023.13834
MLA
Li, D., Liu, L., Li, F., Ma, C., Ge, K."Nifuroxazide induces the apoptosis of human non‑small cell lung cancer cells through the endoplasmic reticulum stress PERK signaling pathway". Oncology Letters 25.6 (2023): 248.
Chicago
Li, D., Liu, L., Li, F., Ma, C., Ge, K."Nifuroxazide induces the apoptosis of human non‑small cell lung cancer cells through the endoplasmic reticulum stress PERK signaling pathway". Oncology Letters 25, no. 6 (2023): 248. https://doi.org/10.3892/ol.2023.13834