ArticleCancer cell international2021
Long non-coding RNA NEAT1 facilitates the growth, migration, and invasion of ovarian cancer cells via the let-7 g/MEST/ATGL axis.
Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Leveraging the germ layer development patterns to predict prognosis and identify MEST as a novel therapeutic target in glioma.Cancer cell international · 2026Article
- Article
- Long Non-Coding RNAs in Ovarian Cancer: Mechanistic Insights and Clinical Applications.Cancers · 2025Review
- Unraveling the extracellular vesicle network: insights into ovarian cancer metastasis and chemoresistance.Molecular cancer · 2024Review
- The Role of Long Non-Coding RNAs in Ovarian Cancer Cells.International journal of molecular sciences · 2024Review
- Evaluating Ovarian Cancer Chemotherapy Response Using Gene Expression Data and Machine Learning.BioMedInformatics · 2024Article
- Molecular Mechanisms of Tumorgenesis and Metastasis of Long Non-coding RNA (lncRNA) NEAT1 in Human Solid Tumors; An Update.Cell biochemistry and biophysics · 2024Review
- LncRNAs-circRNAs as Rising Epigenetic Binary Superstars in Regulating Lipid Metabolic Reprogramming of Cancers.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- The long non-coding RNA NEAT1 promotes the progression of human ovarian cancer through targeting miR-214-3p and regulating angiogenesis.Journal of ovarian research · 2023Article
- Emerging roles of the long non-coding RNA NEAT1 in gynecologic cancers.Journal of cell communication and signaling · 2023Review
- Extracellular vesicles derived from M2-polarized tumor-associated macrophages promote immune escape in ovarian cancer through NEAT1/miR-101-3p/ZEB1/PD-L1 axis.Cancer immunology, immunotherapy : CII · 2023Article
- Review
- SYNCRIP Modulates the Epithelial-Mesenchymal Transition in Hepatocytes and HCC Cells.International journal of molecular sciences · 2022Article
- Adding fuel to the fire: The lipid droplet and its associated proteins in cancer progression.International journal of biological sciences · 2022Review
- Recent Advances on the Role of ATGL in Cancer.Frontiers in oncology · 2022Review
- Downregulated Dual-Specificity Protein Phosphatase 1 in Ovarian Carcinoma: A Comprehensive Study With Multiple Methods.Pathology oncology research : POR · 2022Article
- A ferroptosis-related lncRNA signature predicts prognosis in ovarian cancer patients.Translational cancer research · 2021Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimGrowing evidence indicates a significant role of long non-coding RNA (lncRNA) nuclear-enriched abundant transcript 1 (NEAT1) in ovarian cancer, a frequently occurring malignant tumor in women; however, the possible effects of an interplay of NEAT1 with microRNA (miRNA or miR) let-7 g in ovarian cancer are not known. The current study aimed to investigate the role of the NEAT1/let-7 g axis in the growth, migration, and invasion of ovarian cancer cells and explore underlying mechanisms.
methodsNEAT1 expression levels were examined in clinical tissue samples and cell lines. The relationships between NEAT1, let-7 g, and MEST were then analyzed. Gain- or loss-of-function approaches were used to manipulate NEAT1 and let-7 g. The effects of NEAT1 on cell proliferation, migration, invasion, and apoptosis were evaluated. Mouse xenograft models of ovarian cancer cells were established to verify the function of NEAT1 in vivo.
resultsNEAT1 expression was elevated while let-7 g was decreased in ovarian cancer clinical tissue samples and cell lines. A negative correlation existed between NEAT1 and let-7 g, whereby NEAT1 competitively bound to let-7 g and consequently down-regulate let-7 g expression. By this mechanism, the growth, migration, and invasion of ovarian cancer cells were stimulated. In addition, let-7 g targeted mesoderm specific transcript (MEST) and inhibited its expression, leading to promotion of adipose triglyceride lipase (ATGL) expression and inhibition of ovarian cancer cell growth, migration, and invasion. However, the effect of let-7 g was abolished by overexpression of MEST. Furthermore, silencing of NEAT1 decreased the xenograft tumor growth by decreasing MEST while up-regulating let-7 g and ATGL.
conclusionsCumulatively, the findings demonstrated that NEAT1 could promote malignant phenotypes of ovarian cancer cells by regulating the let-7 g/MEST/ATGL signaling axis. Therefore, NEAT1 can be regarded as an important molecular target and biomarker for ovarian cancer.
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