ArticleFrontiers in oncology2021
Ginsenoside Rh7 Suppresses Proliferation, Migration and Invasion of NSCLC Cells Through Targeting ILF3-AS1 Mediated miR-212/SMAD1 Axis.
Article in Frontiers in oncology, 2021. 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Ginsenoside Rh7 affects β-catenin nuclear translocation by inhibitingInternational journal of medical sciences · 2025Article
- Human disease-related long noncoding RNAs: Impact of ginsenosides.Journal of ginseng research · 2024Review
- Therapeutic Applications of Ginseng Natural Compounds for Health Management.International journal of molecular sciences · 2023Review
- EPLIN-β is a novel substrate of ornithine decarboxylase antizyme 1 and mediates cellular migration.Journal of cell science · 2023Article
- Anti-cancer effect and potential microRNAs targets of ginsenosides against breast cancer.Frontiers in pharmacology · 2022Review
- Long non-coding RNA ILF3-AS1 facilitates hepatocellular carcinoma progression by stabilizing ILF3 mRNA in an mHuman cell · 2021Article
- Comparative Transcriptional Analysis of Pulmonary Arterial Hypertension Associated With Three Different Diseases.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is reported that ginsenosides have a significant anti-tumor effect on a variety of tumors. However, the role and mechanism of Rh7 in non-small cell lung cancer (NSCLC) are unclear. In this study, we aimed to study the anti-tumor effect of Rh7 on the proliferation and progression of NSCLC. Bioinformatics analysis showed that ILF3-AS1 was regulated by ginsenoside Rh7 in NSCLC. Down-regulation of ILF3-AS1 could significantly inhibit the proliferation, metastasis and invasion of NSCLC. In addition, ILF3-AS1 negatively controlled miR-212, which in turn targeted SMAD1 expression, thereby regulating NSCLC cell viability and apoptosis. Our results indicate that ILF3-AS1 can be used as a diagnostic and therapeutic target for non-small cell lung cancer. It is discovered for the first time that ginsenoside Rh7 inhibits the expression of ILF3-AS1 and exerts antitumor effects.
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