ArticleBioengineered2022
LncRNA FLVCR1-AS1 mediates miR-23a-5p/SLC7A11 axis to promote malignant behavior of cervical cancer cells.
Article in Bioengineered, 2022. 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, 22 citations in OpenAlex.
- Analysis of long non-coding RNAs associated with disulfidptosis for prognostic signature and immunotherapy response in uterine corpus endometrial carcinoma.Scientific reports · 2023Trial
- Unraveling the mechanisms of LncRNAs in cervical cancer: a comprehensive review.Cell death discovery · 2025Review
- Non-coding RNAs-regulated SLC7A11 modulates ferroptosis: a new strategy for cancer therapy.Functional & integrative genomics · 2025Review
- CRISPR-based dissection of microRNA-23a ~ 27a ~ 24-2 cluster functionality in hepatocellular carcinoma.Oncogene · 2024Article
- Discovery of the Inhibitor Targeting the SLC7A11/xCT Axis through In Silico and In Vitro Experiments.International journal of molecular sciences · 2024Article
- Article
- Review
- The linear ANRIL transcript P14AS regulates the NF-κB signaling to promote colon cancer progression.Molecular medicine (Cambridge, Mass.) · 2023Article
- The mechanisms and diagnostic potential of lncRNAs, miRNAs, and their related signaling pathways in cervical cancer.Frontiers in cell and developmental biology · 2023Review
- Role and Dysregulation of miRNA in Patients with Parkinson's Disease.International journal of molecular sciences · 2022Article
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cervical cancer (CC) is the most common gynecological malignant tumor in the world. Long non-coding RNA (lncRNAs) plays an important role in cell activities of various cancers including CC. This study aims to reveal the biological function of FLVCR1-AS1 in CC and clarify its possible mechanism of action. The findings suggest that the expression of FLVCR1-AS1 was elevated in CC tissues and cell lines, and that high expression of FLVCR1-AS1 was associated with poor prognosis of CC patients. In addition, knockdown of FLVCR1-AS1 could inhibit the proliferation and migration, invasion and epithelial-mesenchymal transformation (EMT) of CC cells, as well as accelerating apoptosis, to inhibit the development of CC. In addition, via the dual-luciferase reporting assay and RIP assay were confirmed that FLVCR1-AS1 acted as a competitive endogenous RNA to inhibit the expression of microRNA (miR)-23a-5p, and miR-23a-5p targeted the 3'-untranslated region site of Solute carrier family 7 member 11 (SLC7A11) and negatively regulated the expression of SLC7A11. Functional rescue experiments showed that miR-23a-5p inhibitors reversed the inhibitory effect of FLVCR1-AS1-silencing on proliferation, EMT, migration and invasion, and the promoting impact of apoptosis of CC cells. In addition, SLC7A11 rescued the effect of miR-23a-5p overexpression on progression of CC cells. In conclusion, FLVCR1-AS1 is involved in the malignant phenotype of CC cells through miR-23a-5p/SLC7A11 axis, which may provide a beneficial direction for the treatment of CC.
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