lncRNA HIF1A-AS2 acts as an oncogene to regulate malignant phenotypes in cervical cancer
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View abstract on PubMed
Summary
This summary is machine-generated.Long noncoding RNA HIF1A-AS2 promotes cervical cancer (CC) progression by activating c-Jun and sponging miR-34b-5p, making it a potential therapeutic target. This study reveals HIF1A-AS2's oncogenic role in CC.
Area Of Science
- Molecular Oncology
- RNA Biology
- Cancer Genomics
Background
- Long noncoding RNAs (lncRNAs) play roles in cancer, but HIF1A-AS2 mechanisms in cervical cancer (CC) are unclear.
- HIF1A-AS2 is upregulated in various human cancers, suggesting a role in tumor progression.
Purpose Of The Study
- Investigate the expression pattern of HIF1A-AS2 in cervical cancer.
- Elucidate the molecular mechanisms and signaling pathways involving HIF1A-AS2 in CC.
Main Methods
- Assessed HIF1A-AS2 transcript levels in 20 CC patient specimens and 3 CC cell lines using qRT-PCR.
- Performed functional assays (CCK-8, Transwell, Apoptosis) and utilized bioinformatics databases (JASPAR, miRDB, Targetscan).
- Validated interactions using dual luciferase assays, ChIP, and RIP experiments.
Main Results
- HIF1A-AS2 expression was significantly elevated in CC tissues and cell lines.
- HIF1A-AS2 knockdown inhibited proliferation and invasion while inducing apoptosis; overexpression had opposite effects.
- Identified c-Jun as a transcription factor activating HIF1A-AS2 and confirmed HIF1A-AS2 acts as a molecular sponge for miR-34b-5p, targeting radixin (RDX).
Conclusions
- c-Jun-activated HIF1A-AS2 functions as an oncogenic factor in CC by sponging miR-34b-5p to regulate radixin.
- HIF1A-AS2 presents a promising therapeutic target for cervical cancer treatment.
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