ArticleReproductive sciences (Thousand Oaks, Calif.)2021
Circ_0019435 Exerts Its Functions in the Cellular Process of Cervical Cancer via Epigenetically Silencing DKK1 and PTEN.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2021. 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, 7 citations in OpenAlex.
- Emerging landscape of oncogenic signaling pathways in cervical cancer.Discover oncology · 2026Review
- Targeting epigenetic regulators as a promising avenue to overcome cancer therapy resistance.Signal transduction and targeted therapy · 2025Review
- Treating human cancer by targeting EZH2.Genes & diseases · 2025Review
- Circ_0006646 Accelerates the Growth and Metastasis of Cervical Cancer by Elevating RRM2 Through miR-758-3p.Biochemical genetics · 2023Article
- Histone Modifications and Non-Coding RNAs: Mutual Epigenetic Regulation and Role in Pathogenesis.International journal of molecular sciences · 2022Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
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Abstract
Cervical cancer (CC) is the most serious gynecological malignancy among women worldwide. As a subtype of noncoding RNAs (ncRNAs), circular RNAs (circRNAs) play important roles in the regulation of gene expression and cancer progression. It was discovered from the cancer-specific circRNA database (CSCD) that circ_0019435 was mainly distributed in the nucleus of HeLa-S3 cells. However, few researches have mentioned circ_0019435 with its function in cancers. The present study uncovered that circ_0019435 was upregulated in CC cells by qRT-PCR. Moreover, circ_0019435 was more stable than its linear isoform-ABCC2. Besides, no regulation of circ_0019435 on ABCC2 and the chemoresistance of CC cells were found. Then, it was unveiled by a series of functional assays including colony formation, trypan blue staining, and transwell invasion assays in that circ_0019435 ablation induced the suppression of proliferation, invasion, and EMT of HeLa and SiHa cells. The subcellular distribution of circ_0019435 was assessed by subcellular fractionation and FISH assay. Furthermore, it was disclosed that circ_0019435 binds to EZH2 to silence DKK1 and PTEN. Finally, rescue assays corroborated that DKK1 and PTEN were involved in circ_0019435-mediated CC cell progression. In conclusion, circ_0019435 regulates DKK1 and PTEN expression at the epigenetic level, thereby influencing the progression of CC cells.
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