ArticleOncogene2014
LPLUNC1 suppresses IL-6-induced nasopharyngeal carcinoma cell proliferation via inhibiting the Stat3 activation.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
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Who cites it
86 citing papers in PubMed, 129 citations in OpenAlex.
- Nasopharyngeal carcinoma: epidemiology, risk factors, signaling pathways, clinical features, diagnosis, and management.Molecular biomedicine · 2026Review
- A review on the role of IL-6 in the onset and progression of nasopharyngeal carcinoma.Medical oncology (Northwood, London, England) · 2025Review
- mOncogene · 2025Article
- Advances and challenges in drug repurposing in precision therapeutics of colorectal cancer.World journal of gastrointestinal oncology · 2025Review
- BPIFB1, Serving as a Downstream Effector of EBV-miR-BART4, Blocks Immune Escape of Nasopharyngeal Carcinoma via Inhibiting PD-L1 Expression.Biochemical genetics · 2025Article
- Targeting tumor‑associated macrophages: Critical players in tumor progression and therapeutic strategies (Review).International journal of oncology · 2024Review
- Significance of Pre-Treatment CALLY Score Combined with EBV-DNA Levels for Prognostication in Non-Metastatic Nasopharyngeal Cancer Patients: A Clinical Perspective.Journal of inflammation research · 2024Article
- USP7 inhibits the progression of nasopharyngeal carcinoma via promoting SPLUNC1-mediated M1 macrophage polarization through TRIM24.Cell death & disease · 2023Article
- Update on Radiotherapy Changes of Nasopharyngeal Carcinoma Tumor Microenvironment.World journal of oncology · 2023Review
- ZIC2 induces pro-tumor macrophage polarization in nasopharyngeal carcinoma by activating the JUNB/MCSF axis.Cell death & disease · 2023Article
- Exosomal miR-18a-5p promotes EMT and metastasis of NPC cells via targeting BTG3 and activating the Wnt/β-catenin signaling pathway.Cell cycle (Georgetown, Tex.) · 2023Article
- LPLUNC1 reduces glycolysis in nasopharyngeal carcinoma cells through the PHB1-p53/c-Myc axis.Cancer science · 2023Article
- A Microfluidic Platform Revealing Interactions between Leukocytes and Cancer Cells on Topographic Micropatterns.Biosensors · 2022Article
- Therapeutic Approaches Targeting Proteins in Tumor-Associated Macrophages and Their Applications in Cancers.Biomolecules · 2022Review
- BPIFB1 inhibits vasculogenic mimicry via downregulation of GLUT1-mediated H3K27 acetylation in nasopharyngeal carcinoma.Oncogene · 2022Article
- Construction of a lncRNA-mRNA Co-Expression Network for Nasopharyngeal Carcinoma.Frontiers in oncology · 2022Article
- A three-phase trans-ethnic study revealsJournal of gastrointestinal oncology · 2021Article
- Correlation of IL-6 and JAK2/STAT3 signaling pathway with prognosis of nasopharyngeal carcinoma patients.Aging · 2021Article
- Reduced O-GlcNAcylation of SNAP-23 promotes cisplatin resistance by inducing exosome secretion in ovarian cancer.Cell death discovery · 2021Article
- SET knockdown attenuated phenotype modulation and calcium channel associated markers of airway smooth muscle cells in asthmatic mice.Annals of translational medicine · 2021Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor-associated macrophage (TAM)-related chronic inflammation and interleukin-6 (IL-6) contribute to the progression of nasopharyngeal carcinoma (NPC). In this study, we characterized TAMs and IL-6 expression in 212 biopsied NPC and 119 non-tumor nasopharyngeal epithelium (NPE) tissues by tissue array. In comparison with that in the NPE tissues, more TAM infiltrates and a higher density of IL-6 expression were detected in NPC tissues, which were associated with the poor survival of NPC patients. In contrast, little or no LPLUNC1, a regulator of inflammation, expression was detected in NPC tissues, and the levels of LPLUNC1 expression in the NPC were associated negatively with the numbers of TAMs and the levels of IL-6 expression, but positively with the survival of NPC patients. Induction of LPLUNC1 overexpression in NPC cells mitigated lipopolysaccharide (LPS)-induced IL-6, IL-8, tumor necrosis factor-α and IL-1β expression or treatment of THP-1 macrophages with LPLUNC1 inhibited spontaneous and LPS-induced IL-6 expression in vitro. IL-6-promoted NPC cell proliferation in a dose- and time-dependent manner, accompanied by increasing cyclin D1 and Bcl-2 expression and the Stat3 activation, but inhibiting Bax and p21 expression. Induction of LPLUNC1 overexpression inhibited NPC cell proliferation, induced NPC cell arrest, promoted NPC cell apoptosis even after IL-6 stimulation and inhibited the growth of implanted NPC tumors in vivo, which were associated with decreasing cyclin D1 and Bcl-2 expression and the Janus kinase 2 (JAK2)/Stat3 activation, but enhancing Bax and p21 expression. These results suggest that LPLUNC1 can inhibit inflammation and NPC growth by downregulating the Stat3 pathway.
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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.