ArticleMolecular medicine reports2017
Interleukin‑6 induces an epithelial‑mesenchymal transition phenotype in human adamantinomatous craniopharyngioma cells and promotes tumor cell migration.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 66 citations in OpenAlex.
- Blockade of IL-6 signaling prevents paclitaxel-induced neuropathy in C57Bl/6 mice.Cell death & disease · 2020Trial
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- Interrogation of the cellular hierarchies reveals neoplastic evolution and therapeutic vulnerability in craniopharyngioma.Neuro-oncology · 2026Article
- Intratumoral tocilizumab in children with cystic craniopharyngiomas: targeted therapy.Journal of neuro-oncology · 2025Article
- Impaired splicing machinery in craniopharyngiomas unveils PRPF8 and RAVER1 as novel biomarkers and therapeutic targets.Acta neuropathologica communications · 2025Article
- Targeted treatment for craniopharyngioma.Journal of neuro-oncology · 2025Review
- Recent advances in craniopharyngioma pathophysiology and emerging therapeutic approaches.Frontiers in endocrinology · 2025Review
- Solid stress compression enhances breast cancer cell migration through the upregulation of Interleukin-6.Frontiers in cell and developmental biology · 2025Article
- Proteomics study of primary and recurrent adamantinomatous craniopharyngiomas.Clinical proteomics · 2024Article
- Adamantinomatous craniopharyngioma: evolution in the management.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2023Review
- Neural crest E-cadherin loss drives cleft lip/palate by epigenetic modulation via pro-inflammatory gene-environment interaction.Nature communications · 2023Article
- Tocilizumab for the fifth progression of cystic childhood craniopharyngioma-a case report.Frontiers in endocrinology · 2023Article
- Review
- Metastasis and MAPK Pathways.International journal of molecular sciences · 2022Review
- Identification of key pathways and genes in vestibular schwannoma using bioinformatics analysis.Experimental and therapeutic medicine · 2022Article
- Multifaceted Interplay between Hormones, Growth Factors and Hypoxia in the Tumor Microenvironment.Cancers · 2022Review
- Review
- Immune infiltration in aggressive papillary craniopharyngioma: High infiltration but low action.Frontiers in immunology · 2022Article
- Treatment of Cystic Craniopharyngiomas: An Update.Advances and technical standards in neurosurgery · 2022Article
- Cancer-Associated Fibroblasts Regulate the Plasticity of Breast Cancer Stemness through the Production of Leukemia Inhibitory Factor.Life (Basel, Switzerland) · 2021Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Total resection of adamantinomatous craniopharyngioma (ACP) is complex and often leads to postoperative recurrence. This is due to the tendency of the tumor to invade the surrounding brain tissue and the generation of a local inflammatory state between the tumor cells and parenchyma. While there is evidence to suggest that interleukin‑6 (IL‑6) induces craniopharyngioma (CP)‑associated inflammation, particularly in ACP, the role of IL‑6 in the progression of ACP remains unclear. The results of the present study demonstrated that CP inflammation was associated with pathological classification, extent of surgery, degree of calcification and postoperative hypothalamic status scale. Cytokine antibody arrays were conducted to measure the expression of IL‑6 and other inflammatory factors in tumor tissues in response to various levels of inflammatory exposure. IL‑6, IL‑6 receptor (IL‑6R) and glycoprotein 130 expression was detected by immunohistochemistry. In addition, an ELISA was performed to quantify the levels of soluble IL‑6R (sIL‑6R) in the cystic fluid and supernatants of ACP cells and tumor‑associated fibroblasts. These measurements demonstrated that ACP cells produce IL‑6 and its associated proteins. In addition, the results revealed that while the viability of ACP cells was not affected, the migration of ACP cells was promoted by IL‑6 treatment in a concentration‑dependent manner. Conversely, treatment with an IL‑6‑blocking monoclonal antibody significantly decreased the migration of ACP cells. In addition, IL‑6 treatment increased the expression of vimentin and decreased the expression of E‑cadherin in a dose‑dependent manner. The findings of the present study demonstrate that IL‑6 may promote migration in vitro via the classic‑ and trans‑signaling pathways by inducing epithelial‑mesenchymal transition in ACP cell cultures.
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