ZNF750 inhibits the proliferation and invasion of melanoma cells through modulating the Wnt/b-catenin signaling pathway
The abnormal expression of Zinc Finger Protein 750 (ZNF750) has been reported in neoplastic diseases. This study investigated the functional role of ZNF750 in the progression of melanoma. Quantitative real-time PCR and immunohistochemistry (IHC) were performed to detect the expression levels of ZNF7...
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| Veröffentlicht in: | Folia histochemica et cytobiologica 2020, Vol.58 (4), p.255-263 |
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| description | The abnormal expression of Zinc Finger Protein 750 (ZNF750) has been reported in neoplastic diseases. This study investigated the functional role of ZNF750 in the progression of melanoma.
Quantitative real-time PCR and immunohistochemistry (IHC) were performed to detect the expression levels of ZNF750 in patients diagnosed with primary cutaneous malignant melanoma. The correlation between clinical-pathological features and ZNF750 expression were clarified. Cell Counting Kit-8 (CCK-8), colony formation and transwell assays were used to explore the effects of ZNF750 on the proliferation, colony formation, migration and invasion of melanoma cells. Western blot assay was used to evaluate the effects of ZNF750 on regulating epithelial-mesenchymal transition (EMT) related proteins.
ZNF750 expression was down-regulated in human melanoma tissues and cells, and correlated with the clinical-pathological features including tumor size, lymph node metastasis, and Clark classification in patients with melanoma. In addition, overexpression of ZNF750 decreased the proliferation, invasion and suppressed EMT of melanoma cells, whereas ZNF750 depletion showed the opposite effects. Importantly, mechanistic analyses implied that upregulation of ZNF750 inhibited the expression of b-catenin and the downstream targets (cyclin D1, c-Myc, Bcl-2, MMP2 and MMP9), indicating it could block the activation of Wnt/b-catenin pathway. Consistently, knockdown of ZNF750 led to the opposite results.
Together, ZNF750 serves as a tumor suppressor for the development and progression of melanoma through regulating the Wnt/b-catenin pathway. This study confirms the involvement of ZNF750 in melanoma progression and may provide a promising therapeutic target for the treatment of melanoma. |
| doi_str_mv | 10.5603/FHC.a2020.0026 |
| format | Article |
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Quantitative real-time PCR and immunohistochemistry (IHC) were performed to detect the expression levels of ZNF750 in patients diagnosed with primary cutaneous malignant melanoma. The correlation between clinical-pathological features and ZNF750 expression were clarified. Cell Counting Kit-8 (CCK-8), colony formation and transwell assays were used to explore the effects of ZNF750 on the proliferation, colony formation, migration and invasion of melanoma cells. Western blot assay was used to evaluate the effects of ZNF750 on regulating epithelial-mesenchymal transition (EMT) related proteins.
ZNF750 expression was down-regulated in human melanoma tissues and cells, and correlated with the clinical-pathological features including tumor size, lymph node metastasis, and Clark classification in patients with melanoma. In addition, overexpression of ZNF750 decreased the proliferation, invasion and suppressed EMT of melanoma cells, whereas ZNF750 depletion showed the opposite effects. Importantly, mechanistic analyses implied that upregulation of ZNF750 inhibited the expression of b-catenin and the downstream targets (cyclin D1, c-Myc, Bcl-2, MMP2 and MMP9), indicating it could block the activation of Wnt/b-catenin pathway. Consistently, knockdown of ZNF750 led to the opposite results.
Together, ZNF750 serves as a tumor suppressor for the development and progression of melanoma through regulating the Wnt/b-catenin pathway. This study confirms the involvement of ZNF750 in melanoma progression and may provide a promising therapeutic target for the treatment of melanoma.</description><identifier>ISSN: 0239-8508</identifier><identifier>EISSN: 1897-5631</identifier><identifier>DOI: 10.5603/FHC.a2020.0026</identifier><identifier>PMID: 33185885</identifier><language>eng</language><publisher>Poland: Wydawnictwo Via Medica</publisher><subject>Bcl-2 protein ; c-Myc protein ; Cell adhesion & migration ; Cell proliferation ; Cholecystokinin ; Colonies ; Cyclin D1 ; Depletion ; Gelatinase A ; Gelatinase B ; Gene expression ; Immunohistochemistry ; Lymph nodes ; Medical prognosis ; Melanoma ; Membranes ; Mesenchyme ; Metastases ; Metastasis ; Myc protein ; Patients ; Polymerase chain reaction ; Proteins ; Signal transduction ; Skin cancer ; Therapeutic targets ; Tumor suppressor genes ; Tumors ; Wnt protein ; Zinc finger proteins ; β-Catenin</subject><ispartof>Folia histochemica et cytobiologica, 2020, Vol.58 (4), p.255-263</ispartof><rights>2020. This work is published under https://creativecommons.org/licenses/by-nc-nd/4.0 (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2020. This work is published under https://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c266t-9843bf57342b31bcd61e688bbc87e8b76eab000def97b16eb5c539ae1eae9a53</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,4010,27900,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33185885$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Du, Yong</creatorcontrib><creatorcontrib>Lv, Guozhong</creatorcontrib><creatorcontrib>Jing, Changrui</creatorcontrib><creatorcontrib>Liu, Junjie</creatorcontrib><creatorcontrib>Liu, Jing</creatorcontrib><title>ZNF750 inhibits the proliferation and invasion of melanoma cells through modulating the Wnt/b-catenin signaling pathway</title><title>Folia histochemica et cytobiologica</title><addtitle>Folia Histochem Cytobiol</addtitle><description>The abnormal expression of Zinc Finger Protein 750 (ZNF750) has been reported in neoplastic diseases. This study investigated the functional role of ZNF750 in the progression of melanoma.
Quantitative real-time PCR and immunohistochemistry (IHC) were performed to detect the expression levels of ZNF750 in patients diagnosed with primary cutaneous malignant melanoma. The correlation between clinical-pathological features and ZNF750 expression were clarified. Cell Counting Kit-8 (CCK-8), colony formation and transwell assays were used to explore the effects of ZNF750 on the proliferation, colony formation, migration and invasion of melanoma cells. Western blot assay was used to evaluate the effects of ZNF750 on regulating epithelial-mesenchymal transition (EMT) related proteins.
ZNF750 expression was down-regulated in human melanoma tissues and cells, and correlated with the clinical-pathological features including tumor size, lymph node metastasis, and Clark classification in patients with melanoma. In addition, overexpression of ZNF750 decreased the proliferation, invasion and suppressed EMT of melanoma cells, whereas ZNF750 depletion showed the opposite effects. Importantly, mechanistic analyses implied that upregulation of ZNF750 inhibited the expression of b-catenin and the downstream targets (cyclin D1, c-Myc, Bcl-2, MMP2 and MMP9), indicating it could block the activation of Wnt/b-catenin pathway. Consistently, knockdown of ZNF750 led to the opposite results.
Together, ZNF750 serves as a tumor suppressor for the development and progression of melanoma through regulating the Wnt/b-catenin pathway. This study confirms the involvement of ZNF750 in melanoma progression and may provide a promising therapeutic target for the treatment of melanoma.</description><subject>Bcl-2 protein</subject><subject>c-Myc protein</subject><subject>Cell adhesion & migration</subject><subject>Cell proliferation</subject><subject>Cholecystokinin</subject><subject>Colonies</subject><subject>Cyclin D1</subject><subject>Depletion</subject><subject>Gelatinase A</subject><subject>Gelatinase B</subject><subject>Gene expression</subject><subject>Immunohistochemistry</subject><subject>Lymph nodes</subject><subject>Medical prognosis</subject><subject>Melanoma</subject><subject>Membranes</subject><subject>Mesenchyme</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Myc protein</subject><subject>Patients</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>Signal transduction</subject><subject>Skin cancer</subject><subject>Therapeutic 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inhibits the proliferation and invasion of melanoma cells through modulating the Wnt/b-catenin signaling pathway</title><author>Du, Yong ; Lv, Guozhong ; Jing, Changrui ; Liu, Junjie ; Liu, Jing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c266t-9843bf57342b31bcd61e688bbc87e8b76eab000def97b16eb5c539ae1eae9a53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Bcl-2 protein</topic><topic>c-Myc protein</topic><topic>Cell adhesion & migration</topic><topic>Cell proliferation</topic><topic>Cholecystokinin</topic><topic>Colonies</topic><topic>Cyclin D1</topic><topic>Depletion</topic><topic>Gelatinase A</topic><topic>Gelatinase B</topic><topic>Gene expression</topic><topic>Immunohistochemistry</topic><topic>Lymph nodes</topic><topic>Medical prognosis</topic><topic>Melanoma</topic><topic>Membranes</topic><topic>Mesenchyme</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Myc protein</topic><topic>Patients</topic><topic>Polymerase chain reaction</topic><topic>Proteins</topic><topic>Signal transduction</topic><topic>Skin cancer</topic><topic>Therapeutic targets</topic><topic>Tumor suppressor genes</topic><topic>Tumors</topic><topic>Wnt protein</topic><topic>Zinc finger proteins</topic><topic>β-Catenin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Du, Yong</creatorcontrib><creatorcontrib>Lv, Guozhong</creatorcontrib><creatorcontrib>Jing, Changrui</creatorcontrib><creatorcontrib>Liu, Junjie</creatorcontrib><creatorcontrib>Liu, Jing</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Docstoc</collection><collection>Bacteriology Abstracts (Microbiology 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Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Du, Yong</au><au>Lv, Guozhong</au><au>Jing, Changrui</au><au>Liu, Junjie</au><au>Liu, Jing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ZNF750 inhibits the proliferation and invasion of melanoma cells through modulating the Wnt/b-catenin signaling pathway</atitle><jtitle>Folia histochemica et cytobiologica</jtitle><addtitle>Folia Histochem Cytobiol</addtitle><date>2020</date><risdate>2020</risdate><volume>58</volume><issue>4</issue><spage>255</spage><epage>263</epage><pages>255-263</pages><issn>0239-8508</issn><eissn>1897-5631</eissn><abstract>The abnormal expression of Zinc Finger Protein 750 (ZNF750) has been reported in neoplastic diseases. This study investigated the functional role of ZNF750 in the progression of melanoma.
Quantitative real-time PCR and immunohistochemistry (IHC) were performed to detect the expression levels of ZNF750 in patients diagnosed with primary cutaneous malignant melanoma. The correlation between clinical-pathological features and ZNF750 expression were clarified. Cell Counting Kit-8 (CCK-8), colony formation and transwell assays were used to explore the effects of ZNF750 on the proliferation, colony formation, migration and invasion of melanoma cells. Western blot assay was used to evaluate the effects of ZNF750 on regulating epithelial-mesenchymal transition (EMT) related proteins.
ZNF750 expression was down-regulated in human melanoma tissues and cells, and correlated with the clinical-pathological features including tumor size, lymph node metastasis, and Clark classification in patients with melanoma. In addition, overexpression of ZNF750 decreased the proliferation, invasion and suppressed EMT of melanoma cells, whereas ZNF750 depletion showed the opposite effects. Importantly, mechanistic analyses implied that upregulation of ZNF750 inhibited the expression of b-catenin and the downstream targets (cyclin D1, c-Myc, Bcl-2, MMP2 and MMP9), indicating it could block the activation of Wnt/b-catenin pathway. Consistently, knockdown of ZNF750 led to the opposite results.
Together, ZNF750 serves as a tumor suppressor for the development and progression of melanoma through regulating the Wnt/b-catenin pathway. This study confirms the involvement of ZNF750 in melanoma progression and may provide a promising therapeutic target for the treatment of melanoma.</abstract><cop>Poland</cop><pub>Wydawnictwo Via Medica</pub><pmid>33185885</pmid><doi>10.5603/FHC.a2020.0026</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Bcl-2 protein c-Myc protein Cell adhesion & migration Cell proliferation Cholecystokinin Colonies Cyclin D1 Depletion Gelatinase A Gelatinase B Gene expression Immunohistochemistry Lymph nodes Medical prognosis Melanoma Membranes Mesenchyme Metastases Metastasis Myc protein Patients Polymerase chain reaction Proteins Signal transduction Skin cancer Therapeutic targets Tumor suppressor genes Tumors Wnt protein Zinc finger proteins β-Catenin |
| title | ZNF750 inhibits the proliferation and invasion of melanoma cells through modulating the Wnt/b-catenin signaling pathway |
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