ArticleCancer medicine2017
LncRNA UCA1 promotes proliferation and cisplatin resistance of oral squamous cell carcinoma by sunppressing miR-184 expression.
Article in Cancer medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 1 of them a synthesis that pooled it.
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Who cites it
128 citing papers in PubMed, 1 synthesis or guideline pooled it, 208 citations in OpenAlex.
- The dual role of miR-184 in cancer: a systematic review of context-dependent regulation.Molecular biology reports · 2025Pooled it
- Circulating lncRNA as Biomarkers and Therapeutics in Oral Cancer: Silent Scripts with Loud Impact.Molecular biology reports · 2026Review
- Targeting the HIF1A-UCA1-PTBP3 axis: a potential therapeutic strategy for head and neck cancer.BMC cancer · 2025Article
- Vitamin D Reshapes Genomic Hierarchies in Skin Cells: lncRNA-Driven Responses in Carcinoma Versus Transcription Factor-Based Regulation in Healthy Skin.International journal of molecular sciences · 2025Article
- Article
- Long Non-Coding RNAs in Ovarian Cancer: Mechanistic Insights and Clinical Applications.Cancers · 2025Review
- Oral squamous cell carcinoma pharmacological treatment; A long non-coding RNAs (long ncRNAs) story.International journal of molecular and cellular medicine · 2025Review
- Competing endogenous RNAs network dysregulation in oral cancer: a multifaceted perspective on crosstalk and competition.Cancer cell international · 2024Review
- Review
- A Novel Pancreatic Cancer Hypoxia Status Related Gene Signature for Prognosis and Therapeutic Responses.Molecular biotechnology · 2024Review
- Molecular and Therapeutic Roles of Non-Coding RNAs in Oral Cancer-A Review.Molecules (Basel, Switzerland) · 2024Review
- Investigating diagnostic potential of long non-coding RNAs in head and neck squamous cell carcinoma using TCGA database and clinical specimens.Scientific reports · 2024Article
- Role of Epigenetics for the Efficacy of Cisplatin.International journal of molecular sciences · 2024Review
- Novel insights on oral squamous cell carcinoma management using long non-coding RNAs.Oncology research · 2024Review
- RNA N6-methyladenosine (m6A) modification in HNSCC: molecular mechanism and therapeutic potential.Cancer gene therapy · 2023Review
- MicroRNAs as the pivotal regulators of cisplatin resistance in head and neck cancers.Cancer cell international · 2023Review
- Crosstalk between long noncoding RNA and microRNA in Cancer.Cellular oncology (Dordrecht, Netherlands) · 2023Review
- Review
- Molecular Signature of Long Non-Coding RNA Associated with Areca Nut-Induced Head and Neck Cancer.Cells · 2023Article
- SNHG15 enhances cisplatin resistance in lung adenocarcinoma by affecting the DNA repair capacity of cancer cells.Diagnostic pathology · 2023Article
68 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemotherapy resistance has become the main obstacle for the effective treatment of human cancers. Long non-coding RNA urothelial cancer associated 1 (UCA1) is generally regarded as an oncogene in some cancers. However, the function and molecular mechanism of UCA1 implicated in cisplatin (CDDP) chemoresistance of oral squamous cell carcinoma (OSCC) is still not fully established. UCA1 expression in tumor tissues and cells was tested by qRT-PCR. MTT, flow cytometry and caspase-3 activity analysis were explored to evaluate the CDDP sensitivity in OSCC cells. Western blot analysis was used to measure BCL2, Bax and SF1 protein expression. Luciferase reporter assay was conducted to investigate the molecular relationship between UCA1, miR-184, and SF1. Nude mice model was used to confirm the functional role of UCA1 in CDDP resistance in vivo. UCA1 expression was upregulated in OSCC tissues, cell lines, and CDDP resistant OSCC cells. Function analysis revealed that UCA1 facilitated proliferation, enhanced CDDP chemoresistance, and suppressed apoptosis in OSCC cells. Mechanisms investigation indicated that UCA1 could interact with miR-184 to repress its expression. Rescue experiments suggested that downregulation of miR-184 partly reversed the tumor suppression effect and CDDP chemosensitivity of UCA1 knockdown in CDDP-resistant OSCC cells. Moreover, UCA1 could perform as a miR-184 sponge to modulate SF1 expression. The OSCC nude mice model experiments demonstrated that depletion of UCA1 further boosted CDDP-mediated repression effect on tumor growth. UCA1 accelerated proliferation, increased CDDP chemoresistance and restrained apoptosis partly through modulating SF1 via sponging miR-184 in OSCC cells, suggesting that targeting UCA1 may be a potential therapeutic strategy for OSCC patients.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.