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• W2945972989 endingPage "175883591984680" @default.
• W2945972989 startingPage "175883591984680" @default.
• W2945972989 abstract "Background: Leptin is considered a tumorigenic adipokine, suggested to promote tumorigenesis and progression in many cancers. On the other hand, intercellular adhesion molecule-1 (ICAM-1) shows altered expression in a variety of benign and malignant diseases. Histologically, ICAM-1 expression is reported as proportional to cancer stage and considered as a potential diagnosis biomarker. The altered expressions of ICAM-1 and its soluble form in malignant diseases have gained interests in recent years. Material and methods: The expression of ICAM-1 and its regulatory signaling were examined by Western blot or flow cytometry. The effect of soluble ICAM-1 on osteoclast formation was investigated by tartrate-resistance acid phosphatase staining of RAW cells and tumor-induced osteolysis in vivo. Results: In our study, we found that leptin enhanced soluble ICAM-1 production but not surface ICAM-1 expression in lung and breast cancer cells, and this effect was regulated through leptin receptor (ObR), while silencing ObR abrogated leptin-induced soluble ICAM-1 expression. In addition, we revealed that leptin administration provoked the JAK1/2, STAT3, FAK, ERK, and GSK3αβ signaling cascade, leading to the elevation of ICAM-1 expression. Moreover, soluble ICAM-1 secreted by leptin-stimulated cancer cells synergize with the receptor activator of nuclear factor kappa-B ligand (RANKL) in inducing osteoclast formation. Soluble ICAM also enhanced tumor-induced osteolysis in vivo. Conclusion: These findings suggest that soluble ICAM-1 produced under leptin treatment enhances osteoclast formation and is involved in tumor-induced osteolysis. Leptin plays an important role in physiology in health and diseases. Leptin affects immune responses that may induce inflammation and carcinogenesis. Leptin is also considered as a tumorigenic adipokine suggested to promote tumorigenesis and progression in many cancers. On the other hand, intercellular adhesion molecule-1 (ICAM-1) shows altered expression in a variety of benign and malignant diseases. Histologically, ICAM-1 expression is reported to be proportional to cancer stage and considered as a potential diagnosis biomarker. It has been reported that soluble ICAM-1 allows tumor cells to escape from immune recognition and stimulates angiogenesis and tumor growth. The altered expressions of ICAM-1 and its soluble form in malignant diseases have gained interests in recent years. In our study, we found that leptin enhanced soluble ICAM-1 production but not surface ICAM-1 expression in lung and breast cancer cells, and this effect was regulated through leptin receptor (ObR), while silencing ObR abrogated leptin-induced soluble ICAM-1 expression. In addition, we revealed that leptin administration provoked the JAK1/2, STAT3, FAK, ERK, and GSK3αβ signaling cascade, leading to the elevation of ICAM-1 expression. Moreover, soluble ICAM-1 secreted by leptin-stimulated cancer cells synergize with receptor activator of nuclear factor-kappa B ligand in inducing osteoclast formation. Soluble ICAM also enhanced tumor-induced osteolysis in vivo. These findings suggest that soluble ICAM-1 produced under leptin treatment is possibly involved in lung and breast cancer bone metastasis." @default.
• W2945972989 created "2019-05-29" @default.
• W2945972989 creator A5012928424 @default.
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• W2945972989 creator A5073558272 @default.
• W2945972989 date "2019-01-01" @default.
• W2945972989 modified "2023-09-25" @default.
• W2945972989 title "Induction of osteoclast-like cell formation by leptin-induced soluble intercellular adhesion molecule secreted from cancer cells" @default.
• W2945972989 cites W1671590615 @default.
• W2945972989 cites W1803578108 @default.
• W2945972989 cites W1963606252 @default.
• W2945972989 cites W1964082391 @default.
• W2945972989 cites W1967046400 @default.
• W2945972989 cites W1968020290 @default.
• W2945972989 cites W1970607638 @default.
• W2945972989 cites W1973026818 @default.
• W2945972989 cites W1977462838 @default.
• W2945972989 cites W1978383324 @default.
• W2945972989 cites W1979522770 @default.
• W2945972989 cites W1988452171 @default.
• W2945972989 cites W1992215271 @default.
• W2945972989 cites W1992225704 @default.
• W2945972989 cites W2003213153 @default.
• W2945972989 cites W2007120217 @default.
• W2945972989 cites W2007833797 @default.
• W2945972989 cites W2014801577 @default.
• W2945972989 cites W2015349322 @default.
• W2945972989 cites W2022087876 @default.
• W2945972989 cites W2030907370 @default.
• W2945972989 cites W2047487133 @default.
• W2945972989 cites W2050939102 @default.
• W2945972989 cites W2052503070 @default.
• W2945972989 cites W2053072643 @default.
• W2945972989 cites W2054148405 @default.
• W2945972989 cites W2061172198 @default.
• W2945972989 cites W2061207421 @default.
• W2945972989 cites W2070977769 @default.
• W2945972989 cites W2073070336 @default.
• W2945972989 cites W2073570284 @default.
• W2945972989 cites W2085346691 @default.
• W2945972989 cites W2086799367 @default.
• W2945972989 cites W2089939944 @default.
• W2945972989 cites W2094322105 @default.
• W2945972989 cites W2095688781 @default.
• W2945972989 cites W2099540110 @default.
• W2945972989 cites W2101939624 @default.
• W2945972989 cites W2107089469 @default.
• W2945972989 cites W2108520917 @default.
• W2945972989 cites W2114750875 @default.
• W2945972989 cites W2115424192 @default.
• W2945972989 cites W2127666874 @default.
• W2945972989 cites W2129536244 @default.
• W2945972989 cites W2132408993 @default.
• W2945972989 cites W2132670952 @default.
• W2945972989 cites W2133428001 @default.
• W2945972989 cites W2137104812 @default.
• W2945972989 cites W2140457971 @default.
• W2945972989 cites W2140671431 @default.
• W2945972989 cites W2146065336 @default.
• W2945972989 cites W2150720839 @default.
• W2945972989 cites W2151155898 @default.
• W2945972989 cites W2151986591 @default.
• W2945972989 cites W2158208709 @default.
• W2945972989 cites W2160332101 @default.
• W2945972989 cites W2161962336 @default.
• W2945972989 cites W2163210258 @default.
• W2945972989 cites W2167785811 @default.
• W2945972989 cites W2192362726 @default.
• W2945972989 cites W2255938273 @default.
• W2945972989 cites W2309708713 @default.
• W2945972989 cites W2317191028 @default.
• W2945972989 cites W2395038064 @default.
• W2945972989 cites W2403727656 @default.
• W2945972989 cites W2412946572 @default.
• W2945972989 cites W2414120761 @default.
• W2945972989 cites W2414290242 @default.
• W2945972989 cites W2502655412 @default.
• W2945972989 cites W2546806856 @default.
• W2945972989 cites W2562792972 @default.
• W2945972989 cites W2564105294 @default.
• W2945972989 cites W2565688290 @default.
• W2945972989 cites W2580948701 @default.
• W2945972989 cites W2583791937 @default.
• W2945972989 cites W2605181377 @default.
• W2945972989 cites W2606709243 @default.
• W2945972989 cites W2727328964 @default.
• W2945972989 cites W2741865537 @default.
• W2945972989 cites W2752556614 @default.
• W2945972989 cites W2769688031 @default.
• W2945972989 cites W2811337009 @default.
• W2945972989 cites W2890885177 @default.
• W2945972989 cites W305687484 @default.
• W2945972989 doi "https://doi.org/10.1177/1758835919846806" @default.
• W2945972989 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6535721" @default.
• W2945972989 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31205504" @default.

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