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
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

2295-2307

Informations 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.

Auteurs

Yaozong Xia (Y)

School of Clinical Medicine, Chengdu Medical College, Chengdu, China.

Teng Liu (T)

School of Clinical Medicine, Chengdu Medical College, Chengdu, China.
Department of Laboratory Medicine, the First Affiliated Hospital of Chengdu Medical College, Chengdu, China.

Shihua Deng (S)

Department of Laboratory Medicine, the First Affiliated Hospital of Chengdu Medical College, Chengdu, China.

Li Li (L)

School of Clinical Medicine, Chengdu Medical College, Chengdu, China.

Jin Li (J)

School of Clinical Medicine, Chengdu Medical College, Chengdu, China.

Feng Zhang (F)

School of Clinical Medicine, Chengdu Medical College, Chengdu, China.

Shuang He (S)

School of Clinical Medicine, Chengdu Medical College, Chengdu, China.

Wei Yuan (W)

School of Clinical Medicine, Chengdu Medical College, Chengdu, China.

Dongming Wu (D)

School of Clinical Medicine, Chengdu Medical College, Chengdu, China.
Department of Laboratory Medicine, the First Affiliated Hospital of Chengdu Medical College, Chengdu, China.

Ying Xu (Y)

School of Clinical Medicine, Chengdu Medical College, Chengdu, China.
Department of Laboratory Medicine, the First Affiliated Hospital of Chengdu Medical College, Chengdu, China.

Classifications MeSH