ArticleDiscover oncology2025
Viral IL-10 can promote the proliferation, migration and invasion of nasopharyngeal carcinoma cells and inhibit their apoptosis.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- T cell fate regulation in EBV‑associated nasopharyngeal carcinoma (Review).Oncology reports · 2026Review
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5 authors.
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No grant is acknowledged in the PubMed record.
Abstract
purposeNasopharyngeal carcinoma is a common clinical malignant tumour in the nasopharynx. The secretion of vIL-10 by EB virus can promote the development of nasopharyngeal carcinoma. The purpose of this study was to provide a theoretical basis for potential targets and mechanisms of vIL-10 in nasopharyngeal carcinoma.
methodsA total of 100 ng/mL vIL-10 was applied to the nasopharyngeal carcinoma CNE-2 cell line for 48 h, and then whole transcriptome sequencing analysis was performed to identify potential targets and signalling pathways of vIL-10 in nasopharyngeal carcinoma. The effects of vIL-10 on the proliferation, migration, invasion and apoptosis of human nasopharyngeal carcinoma cells were determined by ELISA, Ki67 immunofluorescence, colony formation, transwell migration/invasion, Hoechst 33,258 staining, flow cytometry and other experiments, and the potential effects of vIL-10 on nasopharyngeal carcinoma cells were verified at the cellular level. Western blotting was performed to measure the changes in key factors of the JAK1-STAT3 signalling pathway in nasopharyngeal carcinoma cells after vIL-10 treatment.
resultsThe whole transcriptome gene sequencing results showed that vIL-10 could effectively activate the JAK-STAT signalling pathway and upregulate the expression of JAK1 and STAT3. Moreover, vIL-10 inhibited the apoptosis of nasopharyngeal carcinoma cells, enhanced their migration and invasion capabilities, and further promoted the proliferation of nasopharyngeal carcinoma cells.
conclusionvIL-10 regulates the JAK1-STAT3 signalling pathway, promotes the proliferation of NPC cells, enhances their migration and invasion capabilities, inhibits tumour cell apoptosis, and participates in the progression of nasopharyngeal carcinoma.
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