ArticleCancer management and research2020
LncRNA miR503HG Regulates the Drug Resistance of Recurrent Cervical Squamous Cell Carcinoma Cells by Regulating miR-155/Caspase-3.
Article in Cancer management and research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- The potential role of miR-155 in the tumorigenesis of cervical cancer.Frontiers in cell and developmental biology · 2025Review
- The role of long noncoding RNAs in therapeutic resistance in cervical cancer.Frontiers in cell and developmental biology · 2022Review
- Four Prognosis-Associated lncRNAs Serve as Biomarkers in Ovarian Cancer.Frontiers in genetics · 2021Article
- The Biological Significance of Long noncoding RNAs Dysregulation and their Mechanism of Regulating Signaling Pathways in Cervical Cancer.International journal of molecular and cellular medicine · 2021Review
- DLEU2 participates in lymphovascular invasion and inhibits cervical cancer cell proliferation, migration, and invasion.International journal of clinical and experimental pathology · 2020Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe purpose of this study is to investigate the role of long non-coding RNA (lncRNA) miR503 Host Gene (miR503HG) in cervical squamous cell carcinoma (CSCC).
methodsAnalysis of TCGA dataset revealed that expression levels of miR503HG in CSCC tissues were over 12 times lower than those in non-tumor tissues, indicating its involvement in CSCC.
resultsIn this study, we observed that levels of miR503HG in plasma were significantly lower in CSCC patients than in healthy participants. The cisplatin-based treatment further downregulated miR503HG in both patients and CSCC cells. MiR503HG overexpression in CSCC cells led to the suppression of miR-155 and elevation of Caspase-3, acting as the downstream target of miR-155. Cell apoptosis analysis showed that miR503HG and Caspase-3 overexpression led to an increased cell apoptosis rate under Cisplatin treatment. MiR-155 played the opposite role and attenuated the functions of Caspase-3 and miR503HG overexpression.
conclusionTherefore, miR503HG may regulate the drug resistance of CSCC cells by regulating mir-155/Caspase-3.
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