ArticleInternational journal of molecular medicine2020
Liriopesides B induces apoptosis and cell cycle arrest in human non‑small cell lung cancer cells.
Article in International journal of molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Liriopesides B inhibits proliferation and metastasis and induces apoptosis of oral squamous cell carcinoma via the PI3K/Akt/mTOR signaling pathway.Translational cancer research · 2025Article
- Bojungikki-Tang Augments Pembrolizumab Efficacy in Human PBMC-Injected H460 Tumor-Bearing Mice.Life (Basel, Switzerland) · 2024Article
- Effect of Spicatoside a on Anti-Osteosarcoma MG63 Cells through Reactive Oxygen Species Generation and the Inhibition of the PI3K-AKT-mTOR Pathway.Antioxidants (Basel, Switzerland) · 2024Article
- Natural products targeting autophagy and apoptosis in NSCLC: a novel therapeutic strategy.Frontiers in oncology · 2024Review
- Establishment and characterization of a novel highly malignant lung cancer cell line ZX2021H derived from a metastatic lymph node lesion.Thoracic cancer · 2022Article
- Coronavirus Infection-Associated Cell Death Signaling and Potential Therapeutic Targets.Molecules (Basel, Switzerland) · 2021Review
- Natural Products, Alone or in Combination with FDA-Approved Drugs, to Treat COVID-19 and Lung Cancer.Biomedicines · 2021Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although significant progress has been made in the treatment of lung cancer, it remains the leading cause of cancer‑associated mortality. Liriopesides B (LPB) is a natural product isolated from the tuber of Liriope platyphylla, whose effective substances have exhibited antitumor activity in several types of cancer. However, the functions of LPB in non‑small cell lung cancer (NSCLC) require further investigation. Therefore, the present study aimed to investigate whether LPB influences the pathogenic effects of NSCLC. In the present study, it was demonstrated that LPB reduced proliferation, and induced apoptosis and cell cycle arrest in non‑small cell lung cancer cells. CCK‑8 and colony formation assays demonstrated that LPB decreased cell viability and proliferation of H460 and H1975 cells in a dose‑dependent manner. Flow cytometry revealed that LPB significantly induced apoptosis of NSCLC cells, along with changes in the expression of apoptosis‑associated proteins, including an increase in Bax, caspase‑3, and caspase‑8 expression, and a decrease in Bcl‑2 and Bcl‑xl expression. LPB inhibited the progression of the cell cycle from the G1 to the S phase. Furthermore, autophagy was increased in cells treated with LPB. Finally, the expression of programmed death‑ligand 1 was significantly decreased by LPB. In conclusion, the results of the present study highlight a potential novel strategy for the clinical treatment of NSCLC.
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