ArticleMedical science monitor : international medical journal of experimental and clinical research2017
Silencing nc886, a Non-Coding RNA, Induces Apoptosis of Human Endometrial Cancer Cells-1A In Vitro.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Roles of Small Noncoding Vault RNAs in Intestinal Epithelium Homeostasis and Diseases.International journal of molecular sciences · 2025Review
- Non-coding 886 (Epigenetics · 2024Review
- The Versatile Roles of nc886, a Fascinating and Peculiar Regulatory Non-Coding RNA, in Cancer.International journal of molecular sciences · 2024Review
- Human Vault RNAs: Exploring Their Potential Role in Cellular Metabolism.International journal of molecular sciences · 2024Review
- nc886, an RNA Polymerase III-Transcribed Noncoding RNA Whose Expression Is Dynamic and Regulated by Intriguing Mechanisms.International journal of molecular sciences · 2023Review
- Hypermethylation ofMolecular therapy. Nucleic acids · 2022Article
- Downregulation ofGenes & diseases · 2022Article
- Are We Studying Non-Coding RNAs Correctly? Lessons from nc886.International journal of molecular sciences · 2022Review
- Could Moesin Be a New Marker for Indicating Progression in Endometrial Cancer?Cancer management and research · 2022Article
- Methylation status of nc886 epiallele reflects periconceptional conditions and is associated with glucose metabolism through nc886 RNAs.Clinical epigenetics · 2021Article
- Article
- Pan-cancer chromatin analysis of the human vtRNA genes uncovers their association with cancer biology.F1000Research · 2021Article
- RNA polymerase III transcription as a disease factor.Genes & development · 2020Review
- vtRNA2-1/nc886 Produces a Small RNA That Contributes to Its Tumor Suppression Action through the microRNA Pathway in Prostate Cancer.Non-coding RNA · 2020Article
- Rosmarinic Acid Combined with Adriamycin Induces Apoptosis by Triggering Mitochondria-Mediated Signaling Pathway in HepG2 and Bel-7402 Cells.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Non-Coding RNAs and Endometrial Cancer.Genes · 2018Review
- PKR: A Kinase to Remember.Frontiers in molecular neuroscience · 2018Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND The role that nc886, a non-coding microRNA, plays in human endometrial cancer is unknown. The present study aimed to describe the functional role of nc886 in human endometrial cancer-1A (HEC-1A) cell line, which may provide another target for human endometrial cancer treatment. MATERIAL AND METHODS The expression levels of nv886 in normal human endometrial tissue and the early phase and late phase of human endometrial cancer tissues were determined and compared by fluorescence in situ hybridization (FISH). Small interference RNA (siRNA) was used to inhibit nc886, and cell proliferation was evaluated with the MTT test. mRNA levels of PKR, NF-κB, vascular endothelial growth factor (VEGF), and caspase-3 were determined against glyceraldehyde 3-phosphate dehydrogenase (GAPDH between the HEC-1A control group and the silenced group (nc886 silenced with siRNA) by real-time reverse transcription polymerase chain reaction (RT-PCR). The protein levels of PKR (total and phosphorylated form), NF-κB, VEGF, and caspase-3 were determined against GAPDH by Western blotting, and cell apoptosis was determined by flow cytometry. RESULTS Our results indicated that a higher level of nc886 was expressed in the late phase of human endometrial cancer tissue, less than in the early phase but still higher than in normal human endometrial tissue. After nc886 was silenced, protein levels of p-PKR (phosphorylated PKR) and caspase-3 were increased, whereas NF-κB and VEGF were decreased. CONCLUSIONS The rate of apoptosis in the silenced group was increased and the rate of cell proliferation was slower in comparison to the control.
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