ArticleInternational journal of medical sciences2025
Downregulation of lncRNA MNX1-AS1 promotes the ferroptosis and apoptosis of non-small cell lung cancer.
Article in International journal of medical sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Reduced Expression of LINC01515 Suppresses Proliferation and Invasion of Lung Adenocarcinoma Cells via Modulation of the miR-33a-5p/HMGA2 Signaling Axis.Current medicinal chemistry · 2026Article
- Targeting Oncogenic lncRNA KRT7-AS to Induce Ferroptosis Suppresses Ovarian Cancer Progression.Oncology research · 2026Article
- The Regulatory Role of LncRNAs in Modulating Autophagy and Drug Resistance in Non-Small-Cell Lung Cancer: Focus on Targeted Therapeutic Approaches.Biomolecules · 2025Review
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8 authors.
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Abstract
Non-small cell lung cancer (NSCLC), the main histological type of lung cancer, poses a serious threat to human health. Increasing evidence has shown that long non-coding RNA (lncRNA) MNX1-AS1 is involved in the development and progression of cancers, including lung cancer. Apoptosis and ferroptosis, which are two forms of regulated cell death, can be induced by anti-cancer drugs. However, the roles of MNX1-AS1 in apoptosis and ferroptosis are still unclear. Here, we found that knockdown of MNX1-AS1 promoted the ferroptosis induced by RSL3 in NSCLC cells, with a decrease in cell viability and increases in reactive oxygen species (ROS) and malondialdehyde (MDA) levels. Meanwhile, acridine orange/ethidium bromide (AO/EB) double staining, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay and Annexin V/PI double staining revealed that knockdown of MNX1-AS1 promoted the apoptosis caused by paclitaxel in NSCLC cells. In addition, knockdown of MNX1-AS1 resulted in increased expression of pro-apoptotic protein BAX as well as the cleaved caspase-3 and PARP1, and decreased expression of anti-apoptotic protein Bcl-2. RNA sequencing and quantitative real-time PCR assay identified that the expression of ACSL4 was increased, while the expression of ABCG2 was reduced when MNX1-AS1 was knocked down. Rescue assay showed that ACSL4 and ABCG2 were involved in MNX1-AS1-mediated ferroptosis and apoptosis, respectively. Furthermore, knockdown of MNX1-AS1 increased the sensitivity of NSCLC cells to the combination of RSL3 and paclitaxel. Taken together, our data suggest that MNX1-AS1 might be a potential therapeutic target for lung cancer, especially in combination of ferroptosis and/or apoptosis-inducing drugs.
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