ArticleHeliyon2023
Long noncoding RNA SNHG6 promotes the malignant phenotypes of ovarian cancer cells via miR-543/YAP1 pathway.
Article in Heliyon, 2023. 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.
- Long non-coding RNA SNHG6 promotes the proliferation of PASMCs cells through the miR-429/DUSP1 axis during early/subacute vascular responses to pulmonary embolism.Molecular and cellular biochemistry · 2026Article
- Small Nucleolar RNAs (snoRNAs) in Cancer: From Biogenesis to Clinical Potential.OncoTargets and therapy · 2026Review
- Function and Mechanism of Small Nucleolar RNAs (snoRNAs) and Their Host Genes (SNHGs) in Malignant Tumors.Biomolecules · 2025Review
- Article
- DNA Methylation of a Group of Long Non-Coding RNA Genes at Different Stages of Ovarian Cancer Dissemination.Bulletin of experimental biology and medicine · 2024Article
- LncRNAJournal of biomedical research · 2023Article
- LncRNA SNHG6 role in clinicopathological parameters in cancers.European journal of medical research · 2023Review
Corrections and comments
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Authors and funding
3 authors.
Funding
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Abstract
The long non-coding RNA small nucleolar RNA host gene 6 (SNHG6) acts as an oncogene in several cancers, and is highly expressed in ovarian cancer. MiR-543, a tumor suppressor, was expressed lowly in ovarian cancer. However, whether SNHG6 performed its oncogenic role via miR-543 in ovarian cancer, as well as the underlying mechanism is still not clear. In this study, we showed that the levels of SNHG6 and Yes-associated protein 1 (YAP1) were significantly elevated, while the level of miR-543 was significantly decreased, in ovarian cancer tissues compared with adjacent normal samples. We demonstrated that overexpression of SNHG6 significantly promoted the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of ovarian cancer cells SKOV3 and A2780. Knockdown of SNHG6 showed the opposite effects. MiR-543 level was negatively correlated with the SNHG6 level in ovarian cancer tissues. SHNG6 overexpression significantly inhibited the expression of miR-543, and SHNG6 knockdown significantly elevated the expression of miR-543 in ovarian cancer cells. The effects of SNHG6 on ovarian cancer cells were abrogated by miR-543 mimic, and strengthened by
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