| http://purl.uniprot.org/citations/35401828 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/35401828 | http://www.w3.org/2000/01/rdf-schema#comment | "Background: Insulin-like growth factor 1 receptor (IGF-1R) expression and signaling play important roles in promotion of skin cancer progression. Identification of signaling pathways that regulate IGF-1R is crucial for understanding the pathogenesis and therapeutic treatment of skin cancer. Methods: Molecular, cellular and genetic approaches were used to investigate the function of PINCH-1 in regulation of IGF-1R expression and skin cell behavior. Furthermore, conditional PINCH-1 knockout mouse and carcinogen (7, 12-dimethylbenz[a]anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA))-induced skin cancer model were employed to determine the function of PINCH-1 in regulation of IGF-1R expression and skin carcinogenesis in vivo. Results: Knockdown of PINCH-1 from HaCaT keratinocytes or A431 squamous carcinoma cells diminished IGF-1R levels, suppressed cell proliferation and increased apoptosis. Re-expression of PINCH-1 in PINCH-1 knockdown cells restored IGF-1R expression, cell proliferation and survival. Furthermore, depletion of NEDD4 effectively reversed PINCH-1 deficiency-induced down-regulation of IGF-1R expression, cell proliferation and survival. Conditional knockout of PINCH-1 from keratin 5 (K5) positive keratinocytes in mice, like depletion of PINCH-1 from keratinocytes in culture, reduced the IGF-1R level. Using a mouse model of DMBA/TPA-induced skin cancer, we show that the levels of both PINCH-1 and IGF-1R were significantly increased in response to treatment with the carcinogens. Genetic ablation of PINCH-1 from the epidermis markedly reduced the IGF-1R expression and cell proliferation despite stimulation with DMBA/TPA, resulting in resistance to chemical carcinogen-induced skin cancer initiation and progression. Conclusions: Our results reveal a PINCH-1-NEDD4-IGF-1R signaling axis that is critical for promotion of skin tumorigenesis and suggest a new strategy for therapeutic control of skin cancer progression."xsd:string |
| http://purl.uniprot.org/citations/35401828 | http://purl.org/dc/terms/identifier | "doi:10.7150/thno.70744"xsd:string |
| http://purl.uniprot.org/citations/35401828 | http://purl.uniprot.org/core/author | "Guo L."xsd:string |
| http://purl.uniprot.org/citations/35401828 | http://purl.uniprot.org/core/author | "Wang X."xsd:string |
| http://purl.uniprot.org/citations/35401828 | http://purl.uniprot.org/core/author | "Wang R."xsd:string |
| http://purl.uniprot.org/citations/35401828 | http://purl.uniprot.org/core/author | "Wu C."xsd:string |
| http://purl.uniprot.org/citations/35401828 | http://purl.uniprot.org/core/author | "Zhu M."xsd:string |
| http://purl.uniprot.org/citations/35401828 | http://purl.uniprot.org/core/author | "Jiang K."xsd:string |
| http://purl.uniprot.org/citations/35401828 | http://purl.uniprot.org/core/date | "2022"xsd:gYear |
| http://purl.uniprot.org/citations/35401828 | http://purl.uniprot.org/core/name | "Theranostics"xsd:string |
| http://purl.uniprot.org/citations/35401828 | http://purl.uniprot.org/core/pages | "2613-2630"xsd:string |
| http://purl.uniprot.org/citations/35401828 | http://purl.uniprot.org/core/title | "PINCH-1 promotes IGF-1 receptor expression and skin cancer progression through inhibition of the GRB10-NEDD4 complex."xsd:string |
| http://purl.uniprot.org/citations/35401828 | http://purl.uniprot.org/core/volume | "12"xsd:string |
| http://purl.uniprot.org/citations/35401828 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/35401828 |
| http://purl.uniprot.org/citations/35401828 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/35401828 |
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| http://purl.uniprot.org/uniprot/#_A8CVP4-mappedCitation-35401828 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/35401828 |
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| http://purl.uniprot.org/uniprot/#_Q9D7B2-mappedCitation-35401828 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/35401828 |