NF-κB and EGFR participate in S1PR3-mediated human renal cell carcinomas progression
The bioactive lipid sphingosine 1-phosphate (S1P) is implicated in many pivotal processes for the physiological and pathological actions via activating five types of G-protein-coupled S1P receptors (S1PR1‐5). The role of S1P in renal cell carcinoma (RCC) and its receptor subtype specific mediating m...
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Published in | Biochimica et biophysica acta. Molecular basis of disease Vol. 1868; no. 7; p. 166401 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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Elsevier B.V
01.07.2022
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Abstract | The bioactive lipid sphingosine 1-phosphate (S1P) is implicated in many pivotal processes for the physiological and pathological actions via activating five types of G-protein-coupled S1P receptors (S1PR1‐5). The role of S1P in renal cell carcinoma (RCC) and its receptor subtype specific mediating mechanism are poorly studied. So we focus on the regulatory role of S1P in RCC progression and the receptor subtypes involved in S1P-induced actions, intending to further clarify a novel therapeutic target for RCC. Analysis of The Cancer Genome Atlas (TCGA) databases showed that the patients with high expression of S1PR3 had significantly worse overall than with low expression. We further demonstrated that S1P could promote proliferation, migration, and epithelial-mesenchymal transition (EMT) of renal cancer cells in vitro, and the actions were enhanced with the increase of S1PR3 expression. Meanwhile, the results in animal experiments also showed that S1PR3 could accelerate tumorigenesis and metastasis of RCC. Our study also clarified the mechanism for S1P induced cell proliferation is mediated by S1PR3/Gi/p38/Akt/p65/cyclin D1-CDK4 pathway and the main pathway for migration is S1PR3/Gi/q/ERK/p38/p65. In addition, S1PR3 was involved in epidermal growth factor (EGF)-induced actions by enhancing protein expression, not by transactivation of epidermal growth factor receptor (EGFR). These results also further supported our conclusion that the carcinogenic role of S1P/S1PR3 axis. Thus, our findings provide that S1PR3 may be a promising small molecular therapeutic target for S1PR3 expressed cancers.
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AbstractList | The bioactive lipid sphingosine 1-phosphate (S1P) is implicated in many pivotal processes for the physiological and pathological actions via activating five types of G-protein-coupled S1P receptors (S1PR1-5). The role of S1P in renal cell carcinoma (RCC) and its receptor subtype specific mediating mechanism are poorly studied. So we focus on the regulatory role of S1P in RCC progression and the receptor subtypes involved in S1P-induced actions, intending to further clarify a novel therapeutic target for RCC. Analysis of The Cancer Genome Atlas (TCGA) databases showed that the patients with high expression of S1PR3 had significantly worse overall than with low expression. We further demonstrated that S1P could promote proliferation, migration, and epithelial-mesenchymal transition (EMT) of renal cancer cells in vitro, and the actions were enhanced with the increase of S1PR3 expression. Meanwhile, the results in animal experiments also showed that S1PR3 could accelerate tumorigenesis and metastasis of RCC. Our study also clarified the mechanism for S1P induced cell proliferation is mediated by S1PR3/Gi/p38/Akt/p65/cyclin D1-CDK4 pathway and the main pathway for migration is S1PR3/Gi/q/ERK/p38/p65. In addition, S1PR3 was involved in epidermal growth factor (EGF)-induced actions by enhancing protein expression, not by transactivation of epidermal growth factor receptor (EGFR). These results also further supported our conclusion that the carcinogenic role of S1P/S1PR3 axis. Thus, our findings provide that S1PR3 may be a promising small molecular therapeutic target for S1PR3 expressed cancers. The bioactive lipid sphingosine 1-phosphate (S1P) is implicated in many pivotal processes for the physiological and pathological actions via activating five types of G-protein-coupled S1P receptors (S1PR1‐5). The role of S1P in renal cell carcinoma (RCC) and its receptor subtype specific mediating mechanism are poorly studied. So we focus on the regulatory role of S1P in RCC progression and the receptor subtypes involved in S1P-induced actions, intending to further clarify a novel therapeutic target for RCC. Analysis of The Cancer Genome Atlas (TCGA) databases showed that the patients with high expression of S1PR3 had significantly worse overall than with low expression. We further demonstrated that S1P could promote proliferation, migration, and epithelial-mesenchymal transition (EMT) of renal cancer cells in vitro, and the actions were enhanced with the increase of S1PR3 expression. Meanwhile, the results in animal experiments also showed that S1PR3 could accelerate tumorigenesis and metastasis of RCC. Our study also clarified the mechanism for S1P induced cell proliferation is mediated by S1PR3/Gi/p38/Akt/p65/cyclin D1-CDK4 pathway and the main pathway for migration is S1PR3/Gi/q/ERK/p38/p65. In addition, S1PR3 was involved in epidermal growth factor (EGF)-induced actions by enhancing protein expression, not by transactivation of epidermal growth factor receptor (EGFR). These results also further supported our conclusion that the carcinogenic role of S1P/S1PR3 axis. Thus, our findings provide that S1PR3 may be a promising small molecular therapeutic target for S1PR3 expressed cancers. [Display omitted] |
ArticleNumber | 166401 |
Author | Zhao, Pengfei Yan, Yali Zhang, Yantao Pei, Jingyuan Zhang, Chenyu Damirin, Alatangaole Cao, Ying Bao, Gegentuya |
Author_xml | – sequence: 1 givenname: Yali surname: Yan fullname: Yan, Yali – sequence: 2 givenname: Gegentuya surname: Bao fullname: Bao, Gegentuya – sequence: 3 givenname: Jingyuan surname: Pei fullname: Pei, Jingyuan – sequence: 4 givenname: Ying surname: Cao fullname: Cao, Ying – sequence: 5 givenname: Chenyu surname: Zhang fullname: Zhang, Chenyu – sequence: 6 givenname: Pengfei surname: Zhao fullname: Zhao, Pengfei – sequence: 7 givenname: Yantao surname: Zhang fullname: Zhang, Yantao – sequence: 8 givenname: Alatangaole surname: Damirin fullname: Damirin, Alatangaole email: bigaolle@imu.edu.cn |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35346818$$D View this record in MEDLINE/PubMed |
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Keywords | OS EGF IHC MLC CCK CDK Proliferation EMT EGFR TCGA NF-κB RCC S1P PTX Renal cell carcinoma GPCRs S1PR3 Tumor metastasis |
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SubjectTerms | Animals Carcinoma, Renal Cell - genetics EGFR ErbB Receptors - genetics Female Humans Kidney Neoplasms - genetics Male NF-kappa B NF-κB Proliferation Renal cell carcinoma S1PR3 Sphingosine-1-Phosphate Receptors Tumor metastasis |
Title | NF-κB and EGFR participate in S1PR3-mediated human renal cell carcinomas progression |
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