{"title":"MYO3B 通过介导钙离子-RhoA/ROCK1 信号通路促进子宫内膜癌的癌症进展","authors":"Chunmei Zhang, Huifeng Zhang, Xiaofeng Yang, Sufen Li, Liang Wang, Huancheng Su, Jiaolin Yang, Yuanyuan Ding, Xinglin Zhang, Bao Qiang, Sanyuan Zhang","doi":"10.1007/s00432-024-05940-x","DOIUrl":null,"url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Purpose</h3><p>This study aimed to investigate the effect of MYO3B on endometrial cancer (EC) proliferation and invasion.</p><h3 data-test=\"abstract-sub-heading\">Methods</h3><p>The expression of MYO3B in EC tissues and cells was analyzed using TCGA database, immunohistochemical staining, real-time PCR, and western blot (WB). Cell proliferation was detected by CCK8, Annexin V-APC/PI flow cytometry was used to detect apoptosis, intracellular calcium ion (Ca<sup>2+</sup>) was detected by flow cytometry with Fluo-4 AM fluorescent probe, cell migration by scratch assay, and cell invasion by Transwell assay, and the expression of proteins related to Ca<sup>2+</sup> homeostasis and RhoA/ROCK1 signaling pathway was detected by WB and immunofluorescence staining.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>The expression of MYO3B was an influential factor in EC recurrence, and the expression of MYO3B was significantly up-regulated in EC tissues and cells, but down-regulated in KLE cells, and MYO3B knockdown inhibited the proliferation, migration, and invasion ability of EC cells and promoted apoptosis, suggesting that MYO3B plays a tumor-promoting role in EC. Furthermore, MYO3B knockdown decreased Ca<sup>2+</sup> concentration in EC cells and the RhoA/ROCK1 signaling pathway was inhibited, and the effect of MYO3B knockdown on RhoA/ROCK1 signaling was reversed by treatment with the Calmodulin agonist CALP-2, and the effects of MYO3B knockdown on cell proliferation, migration, and invasion were reversed after treatment with the RhoA agonist U-46,619.</p><h3 data-test=\"abstract-sub-heading\">Conclusion</h3><p>MYO3B promotes the proliferation and migration of endometrial cancer cells via Ca<sup>2+</sup>-RhoA/ROCK1 signaling pathway. High expression of MYO3B may be a biomarker for EC metastasis.</p>","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":"85 1","pages":""},"PeriodicalIF":2.7000,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"MYO3B promotes cancer progression in endometrial cancer by mediating the calcium ion-RhoA/ROCK1 signaling pathway\",\"authors\":\"Chunmei Zhang, Huifeng Zhang, Xiaofeng Yang, Sufen Li, Liang Wang, Huancheng Su, Jiaolin Yang, Yuanyuan Ding, Xinglin Zhang, Bao Qiang, Sanyuan Zhang\",\"doi\":\"10.1007/s00432-024-05940-x\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<h3 data-test=\\\"abstract-sub-heading\\\">Purpose</h3><p>This study aimed to investigate the effect of MYO3B on endometrial cancer (EC) proliferation and invasion.</p><h3 data-test=\\\"abstract-sub-heading\\\">Methods</h3><p>The expression of MYO3B in EC tissues and cells was analyzed using TCGA database, immunohistochemical staining, real-time PCR, and western blot (WB). Cell proliferation was detected by CCK8, Annexin V-APC/PI flow cytometry was used to detect apoptosis, intracellular calcium ion (Ca<sup>2+</sup>) was detected by flow cytometry with Fluo-4 AM fluorescent probe, cell migration by scratch assay, and cell invasion by Transwell assay, and the expression of proteins related to Ca<sup>2+</sup> homeostasis and RhoA/ROCK1 signaling pathway was detected by WB and immunofluorescence staining.</p><h3 data-test=\\\"abstract-sub-heading\\\">Results</h3><p>The expression of MYO3B was an influential factor in EC recurrence, and the expression of MYO3B was significantly up-regulated in EC tissues and cells, but down-regulated in KLE cells, and MYO3B knockdown inhibited the proliferation, migration, and invasion ability of EC cells and promoted apoptosis, suggesting that MYO3B plays a tumor-promoting role in EC. Furthermore, MYO3B knockdown decreased Ca<sup>2+</sup> concentration in EC cells and the RhoA/ROCK1 signaling pathway was inhibited, and the effect of MYO3B knockdown on RhoA/ROCK1 signaling was reversed by treatment with the Calmodulin agonist CALP-2, and the effects of MYO3B knockdown on cell proliferation, migration, and invasion were reversed after treatment with the RhoA agonist U-46,619.</p><h3 data-test=\\\"abstract-sub-heading\\\">Conclusion</h3><p>MYO3B promotes the proliferation and migration of endometrial cancer cells via Ca<sup>2+</sup>-RhoA/ROCK1 signaling pathway. High expression of MYO3B may be a biomarker for EC metastasis.</p>\",\"PeriodicalId\":15118,\"journal\":{\"name\":\"Journal of Cancer Research and Clinical Oncology\",\"volume\":\"85 1\",\"pages\":\"\"},\"PeriodicalIF\":2.7000,\"publicationDate\":\"2024-09-19\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Cancer Research and Clinical Oncology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/s00432-024-05940-x\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Cancer Research and Clinical Oncology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s00432-024-05940-x","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"ONCOLOGY","Score":null,"Total":0}
MYO3B promotes cancer progression in endometrial cancer by mediating the calcium ion-RhoA/ROCK1 signaling pathway
Purpose
This study aimed to investigate the effect of MYO3B on endometrial cancer (EC) proliferation and invasion.
Methods
The expression of MYO3B in EC tissues and cells was analyzed using TCGA database, immunohistochemical staining, real-time PCR, and western blot (WB). Cell proliferation was detected by CCK8, Annexin V-APC/PI flow cytometry was used to detect apoptosis, intracellular calcium ion (Ca2+) was detected by flow cytometry with Fluo-4 AM fluorescent probe, cell migration by scratch assay, and cell invasion by Transwell assay, and the expression of proteins related to Ca2+ homeostasis and RhoA/ROCK1 signaling pathway was detected by WB and immunofluorescence staining.
Results
The expression of MYO3B was an influential factor in EC recurrence, and the expression of MYO3B was significantly up-regulated in EC tissues and cells, but down-regulated in KLE cells, and MYO3B knockdown inhibited the proliferation, migration, and invasion ability of EC cells and promoted apoptosis, suggesting that MYO3B plays a tumor-promoting role in EC. Furthermore, MYO3B knockdown decreased Ca2+ concentration in EC cells and the RhoA/ROCK1 signaling pathway was inhibited, and the effect of MYO3B knockdown on RhoA/ROCK1 signaling was reversed by treatment with the Calmodulin agonist CALP-2, and the effects of MYO3B knockdown on cell proliferation, migration, and invasion were reversed after treatment with the RhoA agonist U-46,619.
Conclusion
MYO3B promotes the proliferation and migration of endometrial cancer cells via Ca2+-RhoA/ROCK1 signaling pathway. High expression of MYO3B may be a biomarker for EC metastasis.
期刊介绍：
The "Journal of Cancer Research and Clinical Oncology" publishes significant and up-to-date articles within the fields of experimental and clinical oncology. The journal, which is chiefly devoted to Original papers, also includes Reviews as well as Editorials and Guest editorials on current, controversial topics. The section Letters to the editors provides a forum for a rapid exchange of comments and information concerning previously published papers and topics of current interest. Meeting reports provide current information on the latest results presented at important congresses.
The following fields are covered: carcinogenesis - etiology, mechanisms; molecular biology; recent developments in tumor therapy; general diagnosis; laboratory diagnosis; diagnostic and experimental pathology; oncologic surgery; and epidemiology.
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