ArticleInternational journal of clinical and experimental pathology2019
Overexpression of BPIFB1 promotes apoptosis and inhibits proliferation via the MEK/ERK signal pathway in nasopharyngeal carcinoma.
Article in International journal of clinical and experimental pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Single cell transcriptional analysis of human adenoids identifies molecular features of airway microfold cells.Mucosal immunology · 2025Article
- BPIFB1, Serving as a Downstream Effector of EBV-miR-BART4, Blocks Immune Escape of Nasopharyngeal Carcinoma via Inhibiting PD-L1 Expression.Biochemical genetics · 2025Article
- Proteomic Evidence for Amyloidogenic Cross-Seeding in Fibrinaloid Microclots.International journal of molecular sciences · 2024Article
- Comparison of the broncoalveolar lavage fluid proteomics between foals and adult horses.PloS one · 2023Article
- Article
- Molecular biology of BPIFB1 and its advances in disease.Annals of translational medicine · 2020Review
- Magnesium in Combinatorial With Valproic Acid Suppressed the Proliferation and Migration of Human Bladder Cancer Cells.Frontiers in oncology · 2020Article
Corrections and comments
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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
Nasopharyngeal carcinoma (NPC) is a respiratory malignant epithelial carcinoma. Research has indicated that bactericidal/permeability-increasing fold-containing protein B1 (BPIFB1), mostly secreted by nasopharyngeal epithelia, is dysregulated in patients with NPC. This study aimed to explore the effects of BPIFB1 inviability, proliferation, apoptosis and its molecular mechanism. To confirm the effects of BPIFB1 on NPC cells, BPIFB1 was overexpressed or silenced in NPC-KT cells after being transfected with BPIFB1 or siBPIFB1 plasmids. The results showed that BPIFB1 overexpression could induce apoptosis and DNA damage in NPC-KT cells, and silenced BPIFB1 had the opposite effects. BPIFB1 overexpression can inhibit the cell cycle by being arrested at the G0/G1 phase and by regulating the MEK/ERK signaling pathway. MEK inhibitor U0126 was used to confirm the effects of BPIFB1 on the MEK/ERK pathway, and U0126 can inverse the effects of siBPIFB1. Additionally, BPIFB1 can enhance the anti-proliferative effect of chemotherapy drugs on NPC-KT cells. All the results indicated that BPIFB1 could be a potential target for the treatment of NPC.
Indexed as
Identifiers
31933752PMC6944003W3005489431What 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.