ArticleInternational journal of clinical and experimental pathology2017
E2F1-directed activation of nc886 mediates drug resistance in cervical cancer cells via regulation of major vault protein.
Article in International journal of clinical and experimental pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Human vault RNAs exhibit diverse expression patterns and inter-locus compensation.bioRxiv : the preprint server for biology · 2026Article
- Investigating the role of exosomal long non-coding RNAs in drug resistance within female reproductive system cancers.Frontiers in cell and developmental biology · 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
- Vault RNAs (vtRNAs): Rediscovered non-coding RNAs with diverse physiological and pathological activities.Genes & diseases · 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
- Small but Powerful: The Human Vault RNAs as Multifaceted Modulators of Pro-Survival Characteristics and Tumorigenesis.Cancers · 2022Review
- Pan-cancer chromatin analysis of the human vtRNA genes uncovers their association with cancer biology.F1000Research · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-coding RNAs are critical regulators of tumor biology. nc886, a recently identified non-coding RNA, is overexpressed in some tumors, but undetected in others. However, the precise role of nc886 remains unclear in cervical cancers. In this study, we found that nc886, major vault protein (MVP), and E2F1 exhibited coordinate expression as they were silenced in normal tissues but overexpressed in cervical cancer tissues. We subsequently demonstrate that nc886 upregulation was a critical response to chemotherapy treatment of cervical cancer cells. Mechanistically, inhibition of nc886 increased chemosensitivity, induced apoptosis, and suppressed the protein expression of MVP, a critical regulator of drug resistance. Furthermore, we identify E2F1 as a key transcription regulator of nc886 that directly interacts and modulates promoter activity. Taken together, we demonstrate that E2F1 sufficiently promotes nc886 transcription and in turn MVP expression to drive drug resistance in cervical cancer cells.
Indexed as
Identifiers
31966795PMC6965946W3027025996What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.