Lanatoside C induces ferroptosis in non-small cell lung cancer
GPX4
Lanatoside C
SLC7A11
ferroptosis
non-small cell lung cancer (NSCLC)
Journal
Translational cancer research
ISSN: 2219-6803
Titre abrégé: Transl Cancer Res
Pays: China
ID NLM: 101585958
Informations de publication
Date de publication:
31 May 2024
31 May 2024
Historique:
received:
13
12
2023
accepted:
11
04
2024
medline:
17
6
2024
pubmed:
17
6
2024
entrez:
17
6
2024
Statut:
ppublish
Résumé
Non-small cell lung cancer (NSCLC) is a common malignant tumor worldwide, remaining resistant to chemotherapy drugs. Lanatoside C can inhibit the growth of cancer cell lines. In this study we aimed to investigate the relationship between lanatoside C and ferroptosis, exploring the possible mechanism in NSCLC. Experiments The results showed that lanatoside C had an inhibitory effect on the growth of A549 cells, and the dose of lanatoside C used in this experiment was set at 0.4 µM for 24 hours. When A549 cells were treated with lanatoside C, the cell viability was decreased observably (P<0.001) and LDH release was significantly enhanced (P<0.01) compared with the control group. However, when A549 cells were treated together with lanatoside C and five different inhibitors, containing ferroptosis inhibitors, necroptosis inhibitors, apoptosis inhibitors, pyroptosis inhibitors, and autophagy inhibitors, the results showed that the viability of A549 cells with lanatoside C and ferrostatin-1 (Fer-1) was reduced (P>0.05) and the LDH release was significantly enhanced (P<0.05). Besides, TEM and confocal microscopy showed that the mitochondria of A549 cells in the lanatoside C group disappeared and the mitochondrial membrane potential decreased. Collectively, lanatoside C could inhibit the proliferation and induce ferroptosis, and have a biological effect on inducing ferroptosis in NSCLC.
Sections du résumé
Background
UNASSIGNED
Non-small cell lung cancer (NSCLC) is a common malignant tumor worldwide, remaining resistant to chemotherapy drugs. Lanatoside C can inhibit the growth of cancer cell lines. In this study we aimed to investigate the relationship between lanatoside C and ferroptosis, exploring the possible mechanism in NSCLC.
Methods
UNASSIGNED
Experiments
Results
UNASSIGNED
The results showed that lanatoside C had an inhibitory effect on the growth of A549 cells, and the dose of lanatoside C used in this experiment was set at 0.4 µM for 24 hours. When A549 cells were treated with lanatoside C, the cell viability was decreased observably (P<0.001) and LDH release was significantly enhanced (P<0.01) compared with the control group. However, when A549 cells were treated together with lanatoside C and five different inhibitors, containing ferroptosis inhibitors, necroptosis inhibitors, apoptosis inhibitors, pyroptosis inhibitors, and autophagy inhibitors, the results showed that the viability of A549 cells with lanatoside C and ferrostatin-1 (Fer-1) was reduced (P>0.05) and the LDH release was significantly enhanced (P<0.05). Besides, TEM and confocal microscopy showed that the mitochondria of A549 cells in the lanatoside C group disappeared and the mitochondrial membrane potential decreased.
Conclusions
UNASSIGNED
Collectively, lanatoside C could inhibit the proliferation and induce ferroptosis, and have a biological effect on inducing ferroptosis in NSCLC.
Identifiants
pubmed: 38881941
doi: 10.21037/tcr-23-2285
pii: tcr-13-05-2295
pmc: PMC11170539
doi:
Types de publication
Journal Article
Langues
eng
Pagination
2295-2307Informations de copyright
2024 Translational Cancer Research. All rights reserved.
Déclaration de conflit d'intérêts
Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tcr.amegroups.com/article/view/10.21037/tcr-23-2285/coif). The authors have no conflicts of interest to declare.