ArticleOncology letters2020
Mechanisms of JAK-STAT signaling pathway mediated by CXCL8 gene silencing on epithelial-mesenchymal transition of human cutaneous melanoma cells.
Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- CXCL8 Drives MMP1 Upregulation and Promotes Metastatic Progression in Oral Cancer Through CXCR1/2-Mediated JAK1/STAT3 Activation.International journal of biological sciences · 2026Article
- Targeting CXCL8 alleviates intestinal epithelial inflammation by suppressing the JAK-STAT pathway.European journal of medical research · 2025Article
- Article
- CMTM4 promotes the motility of colon cancer cells under radiation and is associated with an unfavorable neoadjuvant chemoradiotherapy response and patient survival in rectal cancer.Oncology letters · 2025Article
- Targeting chemokine signaling networks for therapeutics in skeletal disorders.Frontiers in endocrinology · 2025Review
- The Multifaceted Role of the IL-2 Cytokine Family in Melanoma: Mechanisms, Therapeutic Implications, and Immune Modulation.Journal of immunology research · 2025Review
- Effects of Glutamine or Glucose Deprivation on Inflammation and Tight Junction Disruption in Yak Rumen Epithelial Cells.Animals : an open access journal from MDPI · 2024Article
- Article
- Immune escape and metastasis mechanisms in melanoma: breaking down the dichotomy.Frontiers in immunology · 2024Review
- The significance of spread through air spaces in the prognostic assessment model of stage I lung adenocarcinoma and the exploration of its invasion mechanism.Journal of cancer research and clinical oncology · 2023Article
- Phenolic acids and a static magnetic field change the expression of transforming growth factor β isoforms in amelanotic melanoma cells.Molecular biology reports · 2023Article
- Possible Mechanisms of Oxidative Stress-Induced Skin Cellular Senescence, Inflammation, and Cancer and the Therapeutic Potential of Plant Polyphenols.International journal of molecular sciences · 2023Review
- Extracellular RNA in melanoma: Advances, challenges, and opportunities.Frontiers in cell and developmental biology · 2023Review
- Genome-wide screening and immune landscape suggest a potential-m6A-related lncRNA risk signature for predicting prognosis of melanoma.Annals of translational medicine · 2022Article
- Transforming Growth Factor-Beta (TGF-β) Signaling in Cancer-A Betrayal Within.Frontiers in pharmacology · 2022Review
- Association of JAK/STAT genetic variants with cutaneous melanoma.Frontiers in oncology · 2022Article
- CXCL8 in Tumor Biology and Its Implications for Clinical Translation.Frontiers in molecular biosciences · 2022Review
- The Landscape of the Tumor Microenvironment in Skin Cutaneous Melanoma Reveals a Prognostic and Immunotherapeutically Relevant Gene Signature.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Effect of CXCL8 gene silencing-mediated JAK-STAT signaling pathway on epithelial-mesenchymal transition (EMT) of human cutaneous melanoma cells was explored. Eighty patients with cutaneous melanoma were enrolled in the study. Cells were transfected accordingly and divided into five groups: The blank group (human cutaneous melanoma cells), NC group (human cutaneous melanoma cells + blank vector plasmid transfection), CXCL8 siRNA group (human cutaneous melanoma cells + CXCL8 silent expression vector plasmid transfection), AG490 group (human cutaneous melanoma cells + JAK-STAT signal pathway inhibitor transfection), CXCL8 siRNA + AG490 group (human cutaneous melanoma cells + JAK-STAT signaling pathway inhibitor + CXCL8 silent expression vector plasmid transfection). The expression levels of CXCL8, JAK2, STAT3, epithelial cadherin (E-cadherin), neurotrophic cadherin (N-cadherin) and vimentin in tissues and cells were detected by RT-qPCR and western blot analysis. CCK-8 and flow cytometry were used to detect cell proliferation and apoptosis. Compared with adjacent normal tissues, the expression of E-cadherin in human cutaneous melanoma tissues was significantly decreased, whereas the expression of CXCL8, JAK2, STAT3, vimentin and N-cadherin was significantly increased (P<0.05). Compared with the blank group, CXCL8 siRNA group and CXCL8 siRNA + AG490 group had significantly lower expression of CXCL8 (P<0.05). Compared with the blank group, the expression levels of JAK2, STAT3, vimentin and N-cadherin in CXCL8 siRNA group, AG490 group and CXCL8 siRNA + AG490 group were decreased, the expression of E-cadherin was increased, the cell proliferation ability was decreased and apoptosis was increased (P<0.05). Compared with CXCL8 siRNA group, the expression of JAK2, STAT3, vimentin and N-cadherin in CXCL8 siRNA + AG490 group were significantly decreased, the expression of E-cadherin was significantly increased, cell proliferation ability was decreased and apoptosis was increased (P<0.05). In conclusion, CXCL8 gene expression silencing may inhibit EMT and cell proliferation while promoting cell apoptosis of human cutaneous melanoma cells by inhibiting the activation of JAK-STAT signaling pathway.
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