ArticleJournal of cellular and molecular medicine2019
Novel reciprocal interaction of lncRNA HOTAIR and miR-214-3p contribute to the solamargine-inhibited PDPK1 gene expression in human lung cancer.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Functional role of long non-coding RNA MALAT1 and HOTAIR in lung cancer.Non-coding RNA research · 2026Review
- Solamargine inhibited the progression of non-small cell lung cancerEuropean journal of histochemistry : EJH · 2025Article
- High expression of LncRNA HOTAIR is a risk factor for temozolomide resistance in glioblastoma via activation of the miR-214/β-catenin/MGMT pathway.Scientific reports · 2024Article
- LncRNA-miRNA interactions prediction based on meta-path similarity and Gaussian kernel similarity.Journal of cellular and molecular medicine · 2024Article
- Main chemical constituents and mechanism of anti-tumor action of Solanum nigrum L.Cancer medicine · 2024Review
- Multi-Omics Mining of lncRNAs with Biological and Clinical Relevance in Cancer.International journal of molecular sciences · 2023Review
- circ_0000376 knockdown suppresses non-small cell lung cancer cell tumor properties by the miR-545-3p/PDPK1 pathway.Open medicine (Warsaw, Poland) · 2023Article
- Active components of Solanum nigrum and their antitumor effects: a literature review.Frontiers in oncology · 2023Review
- Solamargine induces autophagy-mediated apoptosis and enhances bortezomib activity in multiple myeloma.Clinical and experimental pharmacology & physiology · 2022Article
- Solamargine inhibits the growth of hepatocellular carcinoma and enhances the anticancer effect of sorafenib by regulating HOTTIP-TUG1/miR-4726-5p/MUC1 pathway.Molecular carcinogenesis · 2022Article
- Anticancer activity of glycoalkaloids fromFrontiers in pharmacology · 2022Review
- Circular RNA circCPA4 promotes tumorigenesis by regulating miR-214-3p/TGIF2 in lung cancer.Thoracic cancer · 2021Article
- Exosomal circEIF3K from cancer-associated fibroblast promotes colorectal cancer (CRC) progression via miR-214/PD-L1 axis.BMC cancer · 2021Article
- LncRNA HOTAIR promotes proliferation and inhibits apoptosis by sponging miR-214-3p in HPV16 positive cervical cancer cells.Cancer cell international · 2021Article
- Competing endogenous RNAs in lung cancer.Cancer biology & medicine · 2021Review
- Integrated Analysis of lncRNA-Associated ceRNA Network Identifies Two lncRNA Signatures as a Prognostic Biomarker in Gastric Cancer.Disease markers · 2021Article
- LncRNA KTN1-AS1 promotes the progression of non-small cell lung cancer via sponging of miR-130a-5p and activation of PDPK1.Oncogene · 2020Article
- Non-coding RNAs in cancer: platforms and strategies for investigating the genomic "dark matter".Journal of experimental & clinical cancer research : CR · 2020Review
- Exosomal Long Non-Coding RNAs in Lung Diseases.International journal of molecular sciences · 2020Review
- Novel reciprocal interaction of lncRNA HOTAIR and miR-214-3p contribute to the solamargine-inhibited PDPK1 gene expression in human lung cancer.Journal of cellular and molecular medicine · 2019Article
Corrections and comments
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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
Solamargine (SM) has been shown to have anti-cancer properties. However, the underlying mechanism involved remains undetermined. We showed that SM inhibited the growth of non-small cell lung cancer (NSCLC) cells, which was enhanced in cells with silencing of long non-coding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR), while it overcame by overexpression of HOTAIR. In addition, SM increased the expression of miR-214-3p and inhibited 3-phosphoinositide-dependent protein kinase-1 (PDPK1) gene expression, which was strengthened by miR-214-3p mimics. Intriguingly, HOTAIR could directly bind to miR-214-3p and sequestered miR-214-3p from the target gene PDPK1. Intriguingly, overexpression of PDPK1 overcame the effects of SM on miR-214-3p expressions and neutralized the SM-inhibited cell growth. Similar results were observed in vivo. In summary, our results showed that SM-inhibited NSCLC cell growth through the reciprocal interaction between HOTAIR and miR-214-3p, which ultimately suppressed PDPK1 gene expression. HOTAIR effectively acted as a competing endogenous RNA (ceRNA) to stimulate the expression of target gene PDPK1. These complex interactions and feedback mechanisms contribute to the overall effect of SM. This unveils a novel molecular mechanism underlying the anti-cancer effect of SM in human lung cancer.
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