{"title":"AURKA与TRIM28通过Akt信号通路激活休眠LSCC细胞，促进LSCC转移。","authors":"Liyun Yang, Liang Geng, Xinxin Zhang, Jing Lu, Hao Zhang, Geping Wu, Shuixian Huang","doi":"10.1186/s12935-024-03620-x","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Specific molecular mechanisms by which AURKA promoted LSCC metastasis were still unknown.</p><p><strong>Methods: </strong>Bioinformatic analysis was performed the relationship between TRIM28 and LSCC. Immunohistochemistry, Co-IP assay, Rt-PCR and Western Blot were used to examine the expression of related molecular. Flow cytometry was used to examine cell numbers of G0/G1 phase. Plate colony formation, wound healing, migration, invasion and tail vein injection in nude mice assays were applied to examine the proliferation, movement, migration, invasion and metastasis of LSCC.</p><p><strong>Results: </strong>TRIM28 was significantly correlated with LSCC. TRIM28 highly expressed in LSCC and the high TRIM28 expression was related to TNM stage and poor clinical prognosis. Furthermore, AURKA could regulate TRIM28. In addition, deprivation TRIM28 expression induced LSCC cells into dormant state and inhibited LSCC metastasis. Akt signaling pathway played an essential role in promoting the tumor-promoting effects induced by TRIM28.</p><p><strong>Conclusion: </strong>AURKA mediated TRIM28 to revive dormant LSCC cells via Akt signaling pathway to promote LSCC metastasis, targeting TRIM28 might provide a potential treatment strategy for LSCC.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"2"},"PeriodicalIF":5.3000,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11697802/pdf/","citationCount":"0","resultStr":"{\"title\":\"Interaction of AURKA with TRIM28 revives dormant LSCC cells via Akt signaling pathway to promote LSCC metastasis.\",\"authors\":\"Liyun Yang, Liang Geng, Xinxin Zhang, Jing Lu, Hao Zhang, Geping Wu, Shuixian Huang\",\"doi\":\"10.1186/s12935-024-03620-x\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Specific molecular mechanisms by which AURKA promoted LSCC metastasis were still unknown.</p><p><strong>Methods: </strong>Bioinformatic analysis was performed the relationship between TRIM28 and LSCC. Immunohistochemistry, Co-IP assay, Rt-PCR and Western Blot were used to examine the expression of related molecular. Flow cytometry was used to examine cell numbers of G0/G1 phase. Plate colony formation, wound healing, migration, invasion and tail vein injection in nude mice assays were applied to examine the proliferation, movement, migration, invasion and metastasis of LSCC.</p><p><strong>Results: </strong>TRIM28 was significantly correlated with LSCC. TRIM28 highly expressed in LSCC and the high TRIM28 expression was related to TNM stage and poor clinical prognosis. Furthermore, AURKA could regulate TRIM28. In addition, deprivation TRIM28 expression induced LSCC cells into dormant state and inhibited LSCC metastasis. Akt signaling pathway played an essential role in promoting the tumor-promoting effects induced by TRIM28.</p><p><strong>Conclusion: </strong>AURKA mediated TRIM28 to revive dormant LSCC cells via Akt signaling pathway to promote LSCC metastasis, targeting TRIM28 might provide a potential treatment strategy for LSCC.</p>\",\"PeriodicalId\":9385,\"journal\":{\"name\":\"Cancer Cell International\",\"volume\":\"25 1\",\"pages\":\"2\"},\"PeriodicalIF\":5.3000,\"publicationDate\":\"2025-01-03\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11697802/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cancer Cell International\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1186/s12935-024-03620-x\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer Cell International","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s12935-024-03620-x","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ONCOLOGY","Score":null,"Total":0}
Interaction of AURKA with TRIM28 revives dormant LSCC cells via Akt signaling pathway to promote LSCC metastasis.
Background: Specific molecular mechanisms by which AURKA promoted LSCC metastasis were still unknown.
Methods: Bioinformatic analysis was performed the relationship between TRIM28 and LSCC. Immunohistochemistry, Co-IP assay, Rt-PCR and Western Blot were used to examine the expression of related molecular. Flow cytometry was used to examine cell numbers of G0/G1 phase. Plate colony formation, wound healing, migration, invasion and tail vein injection in nude mice assays were applied to examine the proliferation, movement, migration, invasion and metastasis of LSCC.
Results: TRIM28 was significantly correlated with LSCC. TRIM28 highly expressed in LSCC and the high TRIM28 expression was related to TNM stage and poor clinical prognosis. Furthermore, AURKA could regulate TRIM28. In addition, deprivation TRIM28 expression induced LSCC cells into dormant state and inhibited LSCC metastasis. Akt signaling pathway played an essential role in promoting the tumor-promoting effects induced by TRIM28.
Conclusion: AURKA mediated TRIM28 to revive dormant LSCC cells via Akt signaling pathway to promote LSCC metastasis, targeting TRIM28 might provide a potential treatment strategy for LSCC.
期刊介绍：
Cancer Cell International publishes articles on all aspects of cancer cell biology, originating largely from, but not limited to, work using cell culture techniques.
The journal focuses on novel cancer studies reporting data from biological experiments performed on cells grown in vitro, in two- or three-dimensional systems, and/or in vivo (animal experiments). These types of experiments have provided crucial data in many fields, from cell proliferation and transformation, to epithelial-mesenchymal interaction, to apoptosis, and host immune response to tumors.
Cancer Cell International also considers articles that focus on novel technologies or novel pathways in molecular analysis and on epidemiological studies that may affect patient care, as well as articles reporting translational cancer research studies where in vitro discoveries are bridged to the clinic. As such, the journal is interested in laboratory and animal studies reporting on novel biomarkers of tumor progression and response to therapy and on their applicability to human cancers.
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