ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2023
LncRNA HOTAIR enhances RCC2 to accelerate cervical cancer progression by sponging miR-331-3p.
Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2023. 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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10 citing papers in PubMed, 23 citations in OpenAlex.
- A ferroptosis-related competing endogenous RNA network: HOX transcript antisense intergenic RNA/miR-129-5p/brain and acute leukemia, cytoplasmic axis contributes to the malignant progression of esophageal squamous cell carcinoma.Translational cancer research · 2026Article
- Molecular mechanism of non-coding RNAs-mediated radiosensitivity regulation in colorectal cancer.World journal of gastrointestinal oncology · 2025Review
- LncRNA PGM5-AS1 Impairs the Resistance of Cervical Cancer to Cisplatin by Regulating the Hippo and PI3K-AKT Pathways.Biochemical genetics · 2025Article
- Prognostic value of Linc00662/miR-16-5p/FASN in cervical cancer and regulation of tumor progression.Hereditas · 2025Article
- Prognostic value of circ_0000043/miR-590-5p in cervical cancer and regulation of tumor progression.Discover oncology · 2025Article
- LncRNA-miRNA-mRNA regulatory axes as potential biomarkers in cervical cancer: a comprehensive overview.Molecular biology reports · 2025Review
- The role of long noncoding ribonucleic acids in the central nervous system injury.Molecular and cellular biochemistry · 2024Review
- Expression ofFrontiers in oncology · 2024Article
- Defining new biomarkers for overcoming therapeutical resistance in cervical cancer using lncRNA.Molecular biology reports · 2023Review
- Cancer susceptibility 18 positively regulates NUAK Family Kinase 1 expression to promote migration and invasion via sponging of miR-5586-5p in cervical cancer cells.International journal of immunopathology and pharmacologyArticle
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
purposeLong noncoding RNAs (lncRNAs) have been gradually regarded as influential indicators of various cancers. The present study aimed to identify the effects of lncRNA HOTAIR on cervical cancer progression.
methodsRNA and protein expressions were quantified by RT-qPCR and western blot assays. Fluorescence in situ hybridization (FISH) assay was carried out to examine the intracellular location of HOTAIR. Cancer cell viability and mobility were detected by CCK-8, colony formation, transwell and wound healing assays. Binding relationships between miR-331-3p and HOTAIR/RCC2 were validated by luciferase reporter assay.
resultsRT-qPCR assays showed that HOTAIR levels were notably upregulated in cervical cancer tissues and cell lines. Furthermore, a fluorescence in situ hybridization (FISH) assay suggested that HOTAIR was mostly located in the cytoplasm of cancer cells, indicating a sponging function. CCK-8, colony formation, Transwell and wound-healing assays indicated that knockdown of HOTAIR in HeLa and SiHa cells significantly reduced cell growth, migration and invasion. Subsequently, miR-331-3p was proven to be the target molecule of HOTAIR. In addition, results from Pearson's correlation analysis indicated negative correlation between HOTAIR and miR-331-3p in cervical cancer tissues. HOTAIR negatively modulated miR-331-3p expression. Ultimately, the target gene of miR-331-3p was verified to be RCC2, and miR-331-3p negatively modulated RCC2 expression. In addition, analysis on clinical cervical cancer tissues confirmed the negative correlation between miR-331-3p and RCC2. HOTAIR and RCC2 showed oncogenic functions in HeLa and SiHa cells, while miR-331-3p exerted the reverse effect.
conclusionsHOTAIR plays a carcinogenic role in cervical cancer by targeting the miR-331-3p/RCC2 axis. Moreover, clinical cervical cancer tissues confirmed the negative correlation between miR-331-3p with lncRNA HOTAIR and RCC2. These data suggested an underlying therapeutic target for cervical cancer.
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