ArticleFrontiers in oncology2020
Heterozygous p53-R280T Mutation Enhances the Oncogenicity of NPC Cells Through Activating PI3K-Akt Signaling Pathway.
Article in Frontiers in oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Synergistic Anticancer Activity of HSP70 Inhibitor and Doxorubicin in Gain-of-Function Mutated p53 Breast Cancer Cells.Biomedicines · 2025Article
- Aloe-emodin mediates the inhibitory effect of LncRNA D63785 on the PI3K/Akt/mTOR pathway in nasopharyngeal carcinoma.Frontiers in pharmacology · 2025Article
- FGFR3 alterations in bladder cancer: Sensitivity and resistance to targeted therapies.Cancer communications (London, England) · 2024Review
- The Competition of Yin and Yang: Exploring the Role of Wild-Type and Mutant p53 in Tumor Progression.Biomedicines · 2023Article
- Small biomarkers with massive impacts: PI3K/AKT/mTOR signalling and microRNA crosstalk regulate nasopharyngeal carcinoma.Biomarker research · 2022Review
- The roles of ribosomal proteins in nasopharyngeal cancer: culprits, sentinels or both.Biomarker research · 2021Review
- Identifying 8-mRNAsi Based Signature for Predicting Survival in Patients With Head and Neck Squamous Cell Carcinoma via Machine Learning.Frontiers in genetics · 2020Article
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
A heterozygous point mutation of p53 gene at codon 280 from AGA to ACA (R280T) frequently occurs in nasopharyngeal carcinoma (NPC) cell lines, and about 10% NPC tissues. However, the role of this mutation in the pathogenesis of NPC remains unclear. In this study, we generated p53 knockout (KO) NPC cell lines from CNE2 cells carrying heterozygous p53 R280T (p53-R280T) mutation and C666-1 cells carrying wild-type p53 by CRISPR-Cas9 gene editing system, and found that KO of heterozygous p53-R280T significantly decreased NPC cell proliferation and increased NPC cell apoptosis, whereas KO of wild-type p53 had opposite effects on NPC cell proliferation and apoptosis. Moreover, KO of heterozygous p53-R280T inhibited the anchorage-independent growth and
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