ArticleOncology letters2021
Long non-coding RNA UCA1 enhances cervical cancer cell proliferation and invasion by regulating microRNA-299-3p expression.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Pathogenic Mechanisms in Cervical Cancer: Energy Metabolism, Hypoxia and Therapy.Life (Basel, Switzerland) · 2026Review
- Long noncoding RNA UCA1 knockdown inhibits cisplatin-resistant cervical cancer tumorigenesis via the miR-195-5p/IKBKB axis.Acta biochimica et biophysica Sinica · 2025Article
- LncRNA-miRNA-mRNA regulatory axes as potential biomarkers in cervical cancer: a comprehensive overview.Molecular biology reports · 2025Review
- CircVIRMA enhances cell malignant behavior by governing the miR-452-5p/CREBRF pathway in cervical cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- The Role of Urothelial Cancer-Associated 1 in Gynecological Cancers.Current issues in molecular biology · 2024Review
- Long non-coding RNAs PTENP1, GNG12-AS1, MAGI2-AS3 and MEG3 as tumor suppressors in breast cancer and their associations with clinicopathological parameters.Cancer biomarkers : section A of Disease markers · 2024Article
- Serum LINC00152 and UCA1 in HCV-Induced Hepatocellular Carcinoma: Clinical Significance and Prognostic Value.Biologics : targets & therapy · 2023Article
- Review
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The long non-coding RNA, urothelial cancer-associated 1 (UCA1) is an important regulator in several tumors. However, to the best of our knowledge, the clinical roles of UCA1 in cervical cancer remain unclear. Thus, the present study aimed to investigate the function and mechanism of UCA1 in cervical cancer. Reverse transcription-quantitative PCR analysis was performed to detect UCA1 and microRNA (miR)-299-3p expression in cervical cancer tissues and cell lines. The Cell Counting Kit-8 and Transwell assays were performed to assess cell proliferation and invasion, respectively. Furthermore, the dual-luciferase reporter assay was performed to confirm the association between UCA1 and miR-299-3p. Rescue experiments were performed to determine the mechanism of the UCA1/miR-299-3p axis. The results demonstrated that UCA1 expression was upregulated in cervical cancer tissues and cell lines. Furthermore, overexpression of UCA1 enhanced the proliferation and invasion of cervical cancer cells, the effects of which were reversed following UCA1 knockdown. Notably, UCA1 interacted with miR-299-3p and negatively regulated miR-299-3p expression. In addition, miR-299-3p expression was downregulated in cervical cancer tissues and cell lines. Overexpression of miR-299-3p suppressed the proliferation and invasion of cervical cancer cells, reversing the effects of UCA1 knockdown on cervical cancer cell proliferation. Taken together, the results of the present study suggest that UCA1 promotes cell proliferation and invasion by regulating miR-299-3p expression in cervical cancer.
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