ArticleCell death & disease2020
SOX1 promotes differentiation of nasopharyngeal carcinoma cells by activating retinoid metabolic pathway.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 23 citations in OpenAlex.
- Higher expression of SOX1, miR-155, and miR-21 in the colostrum of SARS-CoV-2-infected mothers.Scientific reports · 2026Article
- Functional roles and clinical potential of SOX1 in cancer as a biomarker and therapeutic target.Discover oncology · 2026Review
- Schistosoma haematobium infection is associated with oncogenic gene expression in Cervical Mucosa, with enhanced effects following treatment: A pilot study.PLoS neglected tropical diseases · 2025Article
- WTAP Regulates SOX1 Expression to Affect the Tumorigenicity of Colorectal Cancer via an mDigestive diseases and sciences · 2025Article
- Demethylzeylasteral inhibits oxidative phosphorylation complex biogenesis by targeting LRPPRC in lung cancer.Journal of Cancer · 2025Article
- Serum Onconeural Antibodies in Dogs and Cats for Early Diagnosis of Cancer.Veterinary medicine (Auckland, N.Z.) · 2025Article
- SOX1 acts as a tumor hypnotist rendering nasopharyngeal carcinoma cells refractory to chemotherapy.Cell death discovery · 2023Article
- Expression and significance of SOX B1 genes in glioblastoma multiforme patients.Journal of cellular and molecular medicine · 2022Article
- SOX14 hypermethylation as a tumour biomarker in cervical cancer.BMC cancer · 2021Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Undifferentiation is a key feature of nasopharyngeal carcinoma (NPC), which presents as a unique opportunity for intervention by differentiation therapy. In this study, we found that SOX1 inhibited proliferation, promoted differentiation, and induced senescence of NPC cells, which depended on its transcriptional function. RNA-Seq-profiling analysis showed that multiple undifferentiated markers of keratin family, including KRT5, KRT13, and KRT19, were reduced in SOX1 overexpressed NPC cells. Interestingly, gene ontology (GO) analysis revealed genes in SOX1 overexpressed cells were enriched in extracellular functions. The data of LC/MS untargeted metabolomics showed that the content of retinoids in SOX1 overexpressed cells and culture medium was both higher than that in the control group. Subsequently, we screened mRNA level of genes in retinoic acid (RA) signaling or metabolic pathway and found that the expression of UDP-glucuronosyltransferases was significantly decreased. Furtherly, UGT2B7 could rescue the differentiation induced by SOX1 overexpression. Inhibition of UGTs by demethylzeylasteral (T-96) could mimic SOX1 to promote the differentiation of NPC cells. Thus, we described a mechanism by which SOX1 regulated the differentiation of NPC cells by activating retinoid metabolic pathway, providing a potential target for differentiation therapy of NPC.
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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.