ArticleCancer science2008
High mobility group box-1-inducible melanoma inhibitory activity is associated with nodal metastasis and lymphangiogenesis in oral squamous cell carcinoma.
Article in Cancer science, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 82 citations in OpenAlex.
- Single-cell analysis reveals that GFAPCell death & disease · 2025Article
- Contributing Role of High Mobility Group Box 1 Signaling in Oral Cancer Development and Therapy.Life (Basel, Switzerland) · 2023Review
- The Prognostic Significance of FOXD1 Expression in Head and Neck Squamous Cell Carcinoma.Journal of personalized medicine · 2023Article
- Article
- Hypoxia and the Receptor for Advanced Glycation End Products (RAGE) Signaling in Cancer.International journal of molecular sciences · 2021Review
- Role of Glycated High Mobility Group Box-1 in Gastric Cancer.International journal of molecular sciences · 2021Article
- RAGE Signaling in Melanoma Tumors.International journal of molecular sciences · 2020Review
- Role and Mechanisms of RAGE-Ligand Complexes and RAGE-Inhibitors in Cancer Progression.International journal of molecular sciences · 2020Review
- MiR-126 Modulates Angiogenesis in Breast Cancer by Targeting VEGF-A -mRNAAsian Pacific journal of cancer prevention : APJCP · 2019Article
- NIPA-like domain containing 1 is a novel tumor-promoting factor in oral squamous cell carcinoma.Journal of cancer research and clinical oncology · 2018Article
- A functional variant at the miRNA binding site in HMGB1 gene is associated with risk of oral squamous cell carcinoma.Oncotarget · 2017Article
- Clinical Value of High Mobility Group Box 1 and the Receptor for Advanced Glycation End-products in Head and Neck Cancer: A Systematic Review.International archives of otorhinolaryngology · 2016Review
- LEM domain containing 1 promotes oral squamous cell carcinoma invasion and endothelial transmigration.British journal of cancer · 2016Article
- Article
- Storkhead box 2 and melanoma inhibitory activity promote oral squamous cell carcinoma progression.Oncotarget · 2016Article
- High Mobility Group Box-1 Promotes Inflammation-Induced Lymphangiogenesis via Toll-Like Receptor 4-Dependent Signalling Pathway.PloS one · 2016Article
- HMGB1 overexpression correlates with poor prognosis in early-stage squamous cervical cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- High-mobility group box 1 expression and lymph node metastasis in intrahepatic cholangiocarcinoma.World journal of gastroenterology · 2015Article
- Immunohistochemical detection of high-mobility group box 1 correlates with resistance of preoperative chemoradiotherapy for lower rectal cancer: a retrospective study.World journal of surgical oncology · 2015Article
- The role of HMGB1-RAGE axis in migration and invasion of hepatocellular carcinoma cell lines.Molecular and cellular biochemistry · 2014Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Melanoma inhibitory activity (MIA) is an 11-kDa secretory protein isolated from malignant melanoma cells that is correlated with invasion and metastasis in various human malignancies. We examined MIA expression in 62 oral squamous cell carcinomas (OSCC) by immunohistochemistry. MIA expression was significantly associated with nodal metastasis (P = 0.00018). MIA expression was also associated with expression of high mobility group box-1 (HMGB1) (P < 0.0001) and lymph vessel density (P < 0.0001). Expression levels of MIA, HMGB1, nuclear factor kB (NFkB) p65 and HMGB1-NFkB p65 binding were significantly higher in a metastatic human OSCC cell line (HSC3) than those in a non-metastatic OSCC cell line (HSC4). Treatment with receptor for advanced glycation end products (RAGE) antisense or small interfering RNA and human recombinant HMGB1 (hrHMGB1) did not affect MIA expression, whereas HMGB1 antisense or siRNA treatment decreased MIA expression in HSC3 cells. Then HMGB1 enhanced MIA expression as an NFkB cofactor but not as a RAGE ligand. MIA neutralization by MIA antibodies increased extracellular signal-related kinase 1/2 phosphorylation, but decreased p38 phosphorylation and the expression of vascular epithelial growth factor (VEGF)-C and -D. Treatment with p38 inihibitor decreased VEGF-C and -D expression in HSC3 cells. These results suggest that MIA expression is enhanced by the interaction of intracellular HMGB1 and NFkBp65 and MIA is closely involved in tumor progression and nodal metastasis by the increments of VEGF-C and VEGF-D in OSCC.
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