ArticleJournal of cancer research and clinical oncology2012
Receptor for advanced glycation end products (RAGE) partially mediates HMGB1-ERKs activation in clear cell renal cell carcinoma.
Article in Journal of cancer research and clinical oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 57 citations in OpenAlex.
- Glycosylation in kidney diseases.Precision clinical medicine · 2025Review
- HMGB1/RAGE axis in tumor development: unraveling its significance.Frontiers in oncology · 2024Review
- Insulin/IGF Axis and the Receptor for Advanced Glycation End Products: Role in Meta-inflammation and Potential in Cancer Therapy.Endocrine reviews · 2023Review
- Antigenic targets in clear cell renal cell carcinoma.Kidney cancer (Clifton, Va.) · 2023Review
- RAGE Inhibitors for Targeted Therapy of Cancer: A Comprehensive Review.International journal of molecular sciences · 2022Review
- Review
- HN1L promotes migration and invasion of breast cancer by up-regulating the expression of HMGB1.Journal of cellular and molecular medicine · 2021Article
- Intratumoral Fibrosis in Facilitating Renal Cancer Aggressiveness: Underlying Mechanisms and Promising Targets.Frontiers in cell and developmental biology · 2021Review
- Role and Mechanisms of RAGE-Ligand Complexes and RAGE-Inhibitors in Cancer Progression.International journal of molecular sciences · 2020Review
- S100B as an Antagonist To Interfere with the Interface Area Flanked by S100A11 and RAGE V Domain.ACS omega · 2018Article
- Article
- Hypoxia driven glycation: Mechanisms and therapeutic opportunities.Seminars in cancer biology · 2018Review
- Overexpression of high mobility group box 1 contributes to progressive clinicopathological features and poor prognosis of human bladder urothelial carcinoma.OncoTargets and therapy · 2018Article
- HMGB1/RAGE axis mediates the apoptosis, invasion, autophagy, and angiogenesis of the renal cell carcinoma.OncoTargets and therapy · 2018Article
- HMGB1 promotes myeloid-derived suppressor cells and renal cell carcinoma immune escape.Oncotarget · 2017Article
- High-Mobility Group Box 1 Disrupts Metabolic Function with Cigarette Smoke Exposure in a Ceramide-Dependent Manner.International journal of molecular sciences · 2017Article
- High-mobility group box 1 inhibits HCO3- absorption in the medullary thick ascending limb through RAGE-Rho-ROCK-mediated inhibition of basolateral Na+/H+ exchange.American journal of physiology. Renal physiology · 2016Article
- The role of high mobility group box 1 (HMGB1) in the pathogenesis of kidney diseases.Acta pharmaceutica Sinica. B · 2016Review
- Serum levels of HMGB1 have a diagnostic role in metastatic renal cell cancer.Cancer biomarkers : section A of Disease markers · 2016Article
- Down-regulation of HMGB1 expression by shRNA constructs inhibits the bioactivity of urothelial carcinoma cell lines via the NF-κB pathway.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo explore the expression of receptor for advanced glycation end products (RAGE) and high-mobility group box-1 (HMGB1) and their role in clear cell renal cell carcinoma (CCRCC) development and progression.
methodsExpression of RAGE and HMGB1 was examined in RCC using tissue microarrays. In vitro, quiescent or RAGE-reduced RCC cells were subjected to treatment with HMGB1 and harvested for detecting ERK1/2 phosphorylation via Western blot. Further cell proliferation, migration and invasion were evaluated by Ki-67 immunostaining, wound healing and matrigel invasion assay, respectively.
results①Elevated co-expression of RAGE and HMGB1 in CCRCC was correlated positively with patients' clinical parameters including tumor size, nuclear Fuhrman grade and clinical stage. ②HMGB1 incubation induced ERK1/2 activation in a time- and dose-dependent manner, which could be completely blocked by U0126 (MEK1/2 inhibitor) and partially reversed by RAGE knockdown. ③RAGE knockdown partially reversed the promoted effect of cell proliferation, migration and invasion induced by HMGB1.
conclusionHMGB1 promotes the development and progression of CCRCC via ERK1/2 activation, which is partially mediated by RAGE.
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Registered trials
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