ArticleOncoTargets and therapy2019
Interaction Of c-Jun And HOTAIR- Increased Expression Of p21 Converge In Polyphyllin I-Inhibited Growth Of Human Lung Cancer Cells.
Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Functional role of long non-coding RNA MALAT1 and HOTAIR in lung cancer.Non-coding RNA research · 2026Review
- Rhizoma Paridis saponins in respiratory diseases: a narrative review of multi-target mechanisms and therapeutic potential.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- The role ofHeliyon · 2024Review
- Review
- Therapeutic effects on cancer of the active ingredients in rhizoma paridis.Frontiers in pharmacology · 2023Review
- RacGAP1 promotes the malignant progression of cervical cancer by regulating AP-1 via miR-192 and p-JNK.Cell death & disease · 2022Article
- Anticancer Effect of Polyphyllin I in Suppressing Stem Cell-Like Properties of Hepatocellular Carcinoma via the AKT/GSK-3Oxidative medicine and cellular longevity · 2022Article
- Polyphyllin I, a lethal partner of Palbociclib, suppresses non-small cell lung cancer through activation of p21/CDK2/Rb pathwayCell cycle (Georgetown, Tex.) · 2021Article
- Targeting M2 Macrophages Alleviates Airway Inflammation and Remodeling in Asthmatic MiceFrontiers in molecular biosciences · 2021Article
- Exosomal Long Non-Coding RNAs in Lung Diseases.International journal of molecular sciences · 2020Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLung cancer is a leading cause of cancer-related death worldwide. Previously we demonstrated that polyphyllin I (PPI), a bioactive component extracted from Paris polyphylla, inhibited the growth of non-small cell lung cancer (NSCLC) cells through the SAPK/JNK-mediated suppressing p65, DNMT1 and EZH2 expressions. However, the molecular mechanism underlying anti-lung cancer effect by PPI still remain elusive. PURPOSE: In this current study, we further explored the molecular mechanism underlying the anti-lung cancer effect of PPI.
methodsMTT, Cell-Light
resultsWe showed that PPI suppressed growth of NSCLC cells. Mechanistically, we observed that PPI reduced expression of HOTAIR, while increased transcription factor c-Jun protein levels. Additionally, PPI also induced protein expression and promoter activity of p21, a cyclin-dependent kinase inhibitor. While exogenously expressed HOTAIR showed no effect on c-Jun levels, silencing of c-Jun significantly reversed the PPI-inhibited HOTAIR expression. Moreover, excessive expressed c-Jun further enhanced PPI-inhibited HOTAIR expression and PPI-induced p21 protein levels. Intriguingly, overexpression of HOTAIR and silencing of c-Jun overcame the PPI-induced p21 protein and promoter activity. Finally, silencing of p21 neutralized the PPI-inhibited cell proliferation. Similar results were also found in one xenograft mouse model.
conclusionOur results demonstrate that PPI inhibits growth of NSCLC cells through regulation of HOTAIR and c-Jun expressions, which lead to induction of p21 gene. The interactions among HOTAIR, c-Jun and p21 regulatory axis converge in the overall anti-lung cancer effect of PPI. This study unveils an additional new mechanism for the anti-lung cancer role of PPI.
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