Wnt/[beta]-catenin signaling is a novel therapeutic target for tumor suppressor CYLD-silenced glioblastoma cells
Tumor suppressor cylindromatosis (CYLD) dysfunction by its downregulation is significantly associated with poor prognosis in patients with glioblastoma (GBM), the most aggressive and malignant type of glioma. However, no effective treatment is currently available for patients with CYLD-downregulated...
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| Veröffentlicht in: | Oncology reports 2023-11, Vol.50 (5), p.1 |
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| creator | Kanemaru, Ayumi Ito, Yuki Yamaoka, Michiko Shirakawa, Yuki Yonemaru, Kou Miyake, Shunsuke Ando, Misaki Ota, Masako Masuda, Takeshi Mukasa, Akitake Li, Jian-Dong Saito, Hideyuki Hide, Takuichiro Jono, Hirofumi |
| description | Tumor suppressor cylindromatosis (CYLD) dysfunction by its downregulation is significantly associated with poor prognosis in patients with glioblastoma (GBM), the most aggressive and malignant type of glioma. However, no effective treatment is currently available for patients with CYLD-downregulated GBM. The aim of the present study was to identify the crucial cell signaling pathways and novel therapeutic targets for CYLD down-regulation in GBM cells. CYLD knockdown in GBM cells induced GBM malignant characteristics, such as proliferation, metastasis, and GBM stem-like cell (GSC) formation. Comprehensive proteomic analysis and RNA sequencing data from the tissues of patients with GBM revealed that Wnt/[beta]-catenin signaling was significantly activated by CYLD knockdown in patients with GBM. Furthermore, a Wnt/[beta]-catenin signaling inhibitor suppressed all CYLD knockdown-induced malignant characteristics of GBM. Taken together, the results of the present study revealed that Wnt/[beta]-catenin signaling is responsible for CYLD silencing-induced GBM malignancy; therefore, targeting Wnt/[beta]-catenin may be effective for the treatment of CYLD-negative patients with GBM with poor prognosis. |
| doi_str_mv | 10.3892/or.2023.8638 |
| format | Article |
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However, no effective treatment is currently available for patients with CYLD-downregulated GBM. The aim of the present study was to identify the crucial cell signaling pathways and novel therapeutic targets for CYLD down-regulation in GBM cells. CYLD knockdown in GBM cells induced GBM malignant characteristics, such as proliferation, metastasis, and GBM stem-like cell (GSC) formation. Comprehensive proteomic analysis and RNA sequencing data from the tissues of patients with GBM revealed that Wnt/[beta]-catenin signaling was significantly activated by CYLD knockdown in patients with GBM. Furthermore, a Wnt/[beta]-catenin signaling inhibitor suppressed all CYLD knockdown-induced malignant characteristics of GBM. Taken together, the results of the present study revealed that Wnt/[beta]-catenin signaling is responsible for CYLD silencing-induced GBM malignancy; therefore, targeting Wnt/[beta]-catenin may be effective for the treatment of CYLD-negative patients with GBM with poor prognosis.</description><identifier>ISSN: 1021-335X</identifier><identifier>DOI: 10.3892/or.2023.8638</identifier><language>eng</language><publisher>Spandidos Publications</publisher><subject>Analysis ; B cells ; Care and treatment ; Cellular signal transduction ; Glioblastoma multiforme ; Health aspects ; Prognosis ; RNA ; RNA sequencing</subject><ispartof>Oncology reports, 2023-11, Vol.50 (5), p.1</ispartof><rights>COPYRIGHT 2023 Spandidos Publications</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids></links><search><creatorcontrib>Kanemaru, Ayumi</creatorcontrib><creatorcontrib>Ito, Yuki</creatorcontrib><creatorcontrib>Yamaoka, Michiko</creatorcontrib><creatorcontrib>Shirakawa, Yuki</creatorcontrib><creatorcontrib>Yonemaru, Kou</creatorcontrib><creatorcontrib>Miyake, Shunsuke</creatorcontrib><creatorcontrib>Ando, Misaki</creatorcontrib><creatorcontrib>Ota, Masako</creatorcontrib><creatorcontrib>Masuda, Takeshi</creatorcontrib><creatorcontrib>Mukasa, Akitake</creatorcontrib><creatorcontrib>Li, Jian-Dong</creatorcontrib><creatorcontrib>Saito, Hideyuki</creatorcontrib><creatorcontrib>Hide, Takuichiro</creatorcontrib><creatorcontrib>Jono, Hirofumi</creatorcontrib><title>Wnt/[beta]-catenin signaling is a novel therapeutic target for tumor suppressor CYLD-silenced glioblastoma cells</title><title>Oncology reports</title><description>Tumor suppressor cylindromatosis (CYLD) dysfunction by its downregulation is significantly associated with poor prognosis in patients with glioblastoma (GBM), the most aggressive and malignant type of glioma. However, no effective treatment is currently available for patients with CYLD-downregulated GBM. The aim of the present study was to identify the crucial cell signaling pathways and novel therapeutic targets for CYLD down-regulation in GBM cells. CYLD knockdown in GBM cells induced GBM malignant characteristics, such as proliferation, metastasis, and GBM stem-like cell (GSC) formation. Comprehensive proteomic analysis and RNA sequencing data from the tissues of patients with GBM revealed that Wnt/[beta]-catenin signaling was significantly activated by CYLD knockdown in patients with GBM. Furthermore, a Wnt/[beta]-catenin signaling inhibitor suppressed all CYLD knockdown-induced malignant characteristics of GBM. Taken together, the results of the present study revealed that Wnt/[beta]-catenin signaling is responsible for CYLD silencing-induced GBM malignancy; therefore, targeting Wnt/[beta]-catenin may be effective for the treatment of CYLD-negative patients with GBM with poor prognosis.</description><subject>Analysis</subject><subject>B cells</subject><subject>Care and treatment</subject><subject>Cellular signal transduction</subject><subject>Glioblastoma multiforme</subject><subject>Health aspects</subject><subject>Prognosis</subject><subject>RNA</subject><subject>RNA sequencing</subject><issn>1021-335X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid/><recordid>eNptkE9LAzEQxXNQsFZvfoCA4G23yWazSY6l_oWCl4KKSMlmJ9tINimb1M_vgh4qyIOZd_i9gXkIXVFSMqmqRRzLilSslA2TJ2hGSUULxvjrGTpP6ZOQSpBGzdD-JeTFewtZfxRGZwgu4OT6oL0LPXYJaxziF3icdzDqPRyyMzjrsYeMbRxxPgzTTIf9foSUJrt6W98WyXkIBjrcexdbr1OOg8YGvE8X6NRqn-Dyd8_R5v5us3os1s8PT6vluuiVrAtlreaCCkarSknCCSGUSl6rWnAtade1wAGgq61pWtu0HWvq2nZcc6VYKySbo-ufs732sHXBxjxqM7hktkshqKJMiHqiyn-oSR0MzsQAdnrkb-DmKLAD7fMuRT-1EkM6Br8BFjJ29g</recordid><startdate>20231101</startdate><enddate>20231101</enddate><creator>Kanemaru, Ayumi</creator><creator>Ito, Yuki</creator><creator>Yamaoka, Michiko</creator><creator>Shirakawa, Yuki</creator><creator>Yonemaru, Kou</creator><creator>Miyake, Shunsuke</creator><creator>Ando, Misaki</creator><creator>Ota, Masako</creator><creator>Masuda, Takeshi</creator><creator>Mukasa, Akitake</creator><creator>Li, Jian-Dong</creator><creator>Saito, Hideyuki</creator><creator>Hide, Takuichiro</creator><creator>Jono, Hirofumi</creator><general>Spandidos Publications</general><scope/></search><sort><creationdate>20231101</creationdate><title>Wnt/[beta]-catenin signaling is a novel therapeutic target for tumor suppressor CYLD-silenced glioblastoma cells</title><author>Kanemaru, Ayumi ; Ito, Yuki ; Yamaoka, Michiko ; Shirakawa, Yuki ; Yonemaru, Kou ; Miyake, Shunsuke ; Ando, Misaki ; Ota, Masako ; Masuda, Takeshi ; Mukasa, Akitake ; Li, Jian-Dong ; Saito, Hideyuki ; Hide, Takuichiro ; Jono, Hirofumi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-g984-9ffa571731229805000118549475a81ddbe5eeed4fc6bf6bd3644fd5a5993b783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Analysis</topic><topic>B cells</topic><topic>Care and treatment</topic><topic>Cellular signal transduction</topic><topic>Glioblastoma multiforme</topic><topic>Health aspects</topic><topic>Prognosis</topic><topic>RNA</topic><topic>RNA sequencing</topic><toplevel>online_resources</toplevel><creatorcontrib>Kanemaru, Ayumi</creatorcontrib><creatorcontrib>Ito, Yuki</creatorcontrib><creatorcontrib>Yamaoka, Michiko</creatorcontrib><creatorcontrib>Shirakawa, Yuki</creatorcontrib><creatorcontrib>Yonemaru, Kou</creatorcontrib><creatorcontrib>Miyake, Shunsuke</creatorcontrib><creatorcontrib>Ando, Misaki</creatorcontrib><creatorcontrib>Ota, Masako</creatorcontrib><creatorcontrib>Masuda, Takeshi</creatorcontrib><creatorcontrib>Mukasa, Akitake</creatorcontrib><creatorcontrib>Li, Jian-Dong</creatorcontrib><creatorcontrib>Saito, Hideyuki</creatorcontrib><creatorcontrib>Hide, Takuichiro</creatorcontrib><creatorcontrib>Jono, Hirofumi</creatorcontrib><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kanemaru, Ayumi</au><au>Ito, Yuki</au><au>Yamaoka, Michiko</au><au>Shirakawa, Yuki</au><au>Yonemaru, Kou</au><au>Miyake, Shunsuke</au><au>Ando, Misaki</au><au>Ota, Masako</au><au>Masuda, Takeshi</au><au>Mukasa, Akitake</au><au>Li, Jian-Dong</au><au>Saito, Hideyuki</au><au>Hide, Takuichiro</au><au>Jono, Hirofumi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Wnt/[beta]-catenin signaling is a novel therapeutic target for tumor suppressor CYLD-silenced glioblastoma cells</atitle><jtitle>Oncology reports</jtitle><date>2023-11-01</date><risdate>2023</risdate><volume>50</volume><issue>5</issue><spage>1</spage><pages>1-</pages><issn>1021-335X</issn><abstract>Tumor suppressor cylindromatosis (CYLD) dysfunction by its downregulation is significantly associated with poor prognosis in patients with glioblastoma (GBM), the most aggressive and malignant type of glioma. However, no effective treatment is currently available for patients with CYLD-downregulated GBM. The aim of the present study was to identify the crucial cell signaling pathways and novel therapeutic targets for CYLD down-regulation in GBM cells. CYLD knockdown in GBM cells induced GBM malignant characteristics, such as proliferation, metastasis, and GBM stem-like cell (GSC) formation. Comprehensive proteomic analysis and RNA sequencing data from the tissues of patients with GBM revealed that Wnt/[beta]-catenin signaling was significantly activated by CYLD knockdown in patients with GBM. Furthermore, a Wnt/[beta]-catenin signaling inhibitor suppressed all CYLD knockdown-induced malignant characteristics of GBM. Taken together, the results of the present study revealed that Wnt/[beta]-catenin signaling is responsible for CYLD silencing-induced GBM malignancy; therefore, targeting Wnt/[beta]-catenin may be effective for the treatment of CYLD-negative patients with GBM with poor prognosis.</abstract><pub>Spandidos Publications</pub><doi>10.3892/or.2023.8638</doi></addata></record> |
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| ispartof | Oncology reports, 2023-11, Vol.50 (5), p.1 |
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| language | eng |
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| source | EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Analysis B cells Care and treatment Cellular signal transduction Glioblastoma multiforme Health aspects Prognosis RNA RNA sequencing |
| title | Wnt/[beta]-catenin signaling is a novel therapeutic target for tumor suppressor CYLD-silenced glioblastoma cells |
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