FGFRL1 Promotes Ovarian Cancer Progression by Crosstalk with Hedgehog Signaling
Fibroblast growth factor receptor-like-1 (FGFRL1) has been identified as the fifth fibroblast growth factor receptor. So far, little is known about its biological functions, particularly in cancer development. Here, for the first time, we demonstrated the roles of FGFRL1 in ovarian carcinoma (OC). A...
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| Format: | Article |
| Language: | English |
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Wiley
2018-01-01
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| Series: | Journal of Immunology Research |
| Online Access: | http://dx.doi.org/10.1155/2018/7438608 |
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| _version_ | 1832556937054519296 |
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| author | Haiyan Tai Zhiyong Wu Su’an Sun Zhigang Zhang Congjian Xu |
| author_facet | Haiyan Tai Zhiyong Wu Su’an Sun Zhigang Zhang Congjian Xu |
| author_sort | Haiyan Tai |
| collection | DOAJ |
| description | Fibroblast growth factor receptor-like-1 (FGFRL1) has been identified as the fifth fibroblast growth factor receptor. So far, little is known about its biological functions, particularly in cancer development. Here, for the first time, we demonstrated the roles of FGFRL1 in ovarian carcinoma (OC). An array and existing databases were used to investigate the expression profile of FGFRL1 and the relationship between FGFRL1 expression and clinicopathological parameters. FGFRL1 was significantly upregulated in OC patients, and high FGFRL1 expression was correlated with poor prognosis. In vitro cell proliferation, apoptosis and migration assays, and in vivo subcutaneous xenograft tumor models were used to determine the role of FGFRL1. Loss of function of FGFRL1 significantly influenced cell proliferation, apoptosis, and migration of OC cells in vitro and tumor growth in vivo. Chromatin immunoprecipitation PCR analysis and microarray hybridization were performed to uncover the mechanism. FGFRL1 expression could be induced by hypoxia through hypoxia-inducible factor 1α, which directly binds to the promoter elements of FGFRL1. FGFRL1 promoted tumor progression by crosstalk with Hedgehog (Hh) signaling. Taken together, FGFRL1 is a potential predictor and plays an important role in tumor growth and Hh signaling which could serve as potential therapeutic targets for the treatment of OC. |
| format | Article |
| id | doaj-art-13a9c015eb544bffbc0cbe92126f927c |
| institution | Kabale University |
| issn | 2314-8861 2314-7156 |
| language | English |
| publishDate | 2018-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of Immunology Research |
| spelling | doaj-art-13a9c015eb544bffbc0cbe92126f927c2025-02-03T05:44:03ZengWileyJournal of Immunology Research2314-88612314-71562018-01-01201810.1155/2018/74386087438608FGFRL1 Promotes Ovarian Cancer Progression by Crosstalk with Hedgehog SignalingHaiyan Tai0Zhiyong Wu1Su’an Sun2Zhigang Zhang3Congjian Xu4Obstetrics and Gynecology Hospital, Fudan University, Shanghai 200011, ChinaObstetrics and Gynecology Hospital, Fudan University, Shanghai 200011, ChinaDepartment of Pathology, The First Hospital of Huai’an City, Nanjing Medical University, Huai’an, 223001 Jiangsu, ChinaState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Shanghai Jiao Tong University, Shanghai 200240, ChinaObstetrics and Gynecology Hospital, Fudan University, Shanghai 200011, ChinaFibroblast growth factor receptor-like-1 (FGFRL1) has been identified as the fifth fibroblast growth factor receptor. So far, little is known about its biological functions, particularly in cancer development. Here, for the first time, we demonstrated the roles of FGFRL1 in ovarian carcinoma (OC). An array and existing databases were used to investigate the expression profile of FGFRL1 and the relationship between FGFRL1 expression and clinicopathological parameters. FGFRL1 was significantly upregulated in OC patients, and high FGFRL1 expression was correlated with poor prognosis. In vitro cell proliferation, apoptosis and migration assays, and in vivo subcutaneous xenograft tumor models were used to determine the role of FGFRL1. Loss of function of FGFRL1 significantly influenced cell proliferation, apoptosis, and migration of OC cells in vitro and tumor growth in vivo. Chromatin immunoprecipitation PCR analysis and microarray hybridization were performed to uncover the mechanism. FGFRL1 expression could be induced by hypoxia through hypoxia-inducible factor 1α, which directly binds to the promoter elements of FGFRL1. FGFRL1 promoted tumor progression by crosstalk with Hedgehog (Hh) signaling. Taken together, FGFRL1 is a potential predictor and plays an important role in tumor growth and Hh signaling which could serve as potential therapeutic targets for the treatment of OC.http://dx.doi.org/10.1155/2018/7438608 |
| spellingShingle | Haiyan Tai Zhiyong Wu Su’an Sun Zhigang Zhang Congjian Xu FGFRL1 Promotes Ovarian Cancer Progression by Crosstalk with Hedgehog Signaling Journal of Immunology Research |
| title | FGFRL1 Promotes Ovarian Cancer Progression by Crosstalk with Hedgehog Signaling |
| title_full | FGFRL1 Promotes Ovarian Cancer Progression by Crosstalk with Hedgehog Signaling |
| title_fullStr | FGFRL1 Promotes Ovarian Cancer Progression by Crosstalk with Hedgehog Signaling |
| title_full_unstemmed | FGFRL1 Promotes Ovarian Cancer Progression by Crosstalk with Hedgehog Signaling |
| title_short | FGFRL1 Promotes Ovarian Cancer Progression by Crosstalk with Hedgehog Signaling |
| title_sort | fgfrl1 promotes ovarian cancer progression by crosstalk with hedgehog signaling |
| url | http://dx.doi.org/10.1155/2018/7438608 |
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