Piwi-interacting RNA-651 promotes cell proliferation and migration and inhibits apoptosis in breast cancer by facilitating DNMT1-mediated PTEN promoter methylation
Autor: | Xin He, Ting Liu, Qi Zhou, Miao Li, Jue Jiang, Juan Wang, Lei Sun |
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Rok vydání: | 2021 |
Předmět: |
Adult
DNA (Cytosine-5-)-Methyltransferase 1 Piwi-interacting RNA Apoptosis Breast Neoplasms medicine.disease_cause DNA methyltransferase Epigenesis Genetic Cyclin D1 Cell Movement Cell Line Tumor medicine Humans Gene silencing Tensin PTEN Neoplasm Invasiveness RNA Small Interfering Promoter Regions Genetic Molecular Biology Cell Proliferation biology Cell growth PTEN Phosphohydrolase Cell Biology DNA Methylation Middle Aged Gene Expression Regulation Neoplastic Cancer research biology.protein Female Carcinogenesis Signal Transduction Research Paper Developmental Biology |
Zdroj: | Cell Cycle |
ISSN: | 1551-4005 1538-4101 |
Popis: | Piwi-interacting RNAs (piRNAs/piRs) are small non-coding RNAs that play important roles in stablizing genome through silencing transposable genetic elements. The piR-651 was reported to be dysregulated in several human solid cancer tissues, such as gastric and lung cancers. However, the role of piRNA-651 in carcinogenesis of breast cancer has not been defined. We found that piR-651 was highly expressed in breast cancer tissues and cell lines. Overexpression of piR-651 facilitated cell proliferation and invasion, restrained cell apoptosis and the percentage of arrested cells in G0/G1 phase, accompanied by upregulated expression of oncogenes (MDM2, CDK4 and Cyclin D1), whereas piR-651 downregulation showed the opposite effects. Additionally, piR-651 could promote phosphatase and tensin homolog (PTEN) methylation and its downregulated expression by recruiting DNA methyltransferase 1 (DNMT1) to the PTEN promoter region through complex formation with PIWIL2. PTEN overexpression reversed the effects of upregulated piR-651 on cell functions. This study reveals that piR-651 promotes proliferation and migration and induces apoptosis of breast cancer cells by facilitating DNMT1-mediated PTEN promoter methylation, which may provide a potential therapeutic mechanism for breast cancer. |
Databáze: | OpenAIRE |
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