Hong Zhi, Tana, Nigemutu Bai, Wuenbilige Bai, Bowen Bai, Suo Liu
{"title":"usp22介导的PNMA5去泛素化促进前列腺癌细胞的增殖、迁移和侵袭。","authors":"Hong Zhi, Tana, Nigemutu Bai, Wuenbilige Bai, Bowen Bai, Suo Liu","doi":"10.1016/j.acthis.2025.152279","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Prostate cancer (PCa) stands as one of the primary contributors to cancer-related mortality among men globally. It is reported that USP22 functions as an oncogene, while PNMA5 exhibits a significant pro-metastatic effect. This research investigation centered on examining the interplay between USP22 and PNMA5 and their collaborative role in enhancing PCa progression.</p><p><strong>Methods: </strong>The expression of USP22 and PNMA5 in tissue was determined by IHC. The differential expression of cellular USP22 and PNMA5 were detected using qPCR and immunoblotting, respectively. Cell viability and proliferation were assessed by MTT and sphere-formation assay. Transwell and wound-healing assay were conducted to evaluate the metastatic ability. The interaction between USP22 and PNMA5 was detected by Co-IP and IP. A tumor-bearing mice model was established for in vivo detection.</p><p><strong>Results: </strong>USP22 and PNMA5 were highly expressed in both PCa tumor tissues and cells. Knocking down USP22 or PNMA5 inhibited the migration and invasion of PCa cells. USP22 mediated the deubiquitination of PNMA5. PNMA5 overexpression reversed the decrease in cell viability and proliferation rate, as well as the diminished migration and invasion ability induced by USP22 knockdown.</p><p><strong>Conclusion: </strong>USP22 promotes migration and invasion of PCa cells by regulating PNMA5 deubiquitination.</p>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"127 3","pages":"152279"},"PeriodicalIF":2.4000,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"USP22-mediated PNMA5 deubiquitination promotes proliferation, migration and invasion of prostate cancer cells.\",\"authors\":\"Hong Zhi, Tana, Nigemutu Bai, Wuenbilige Bai, Bowen Bai, Suo Liu\",\"doi\":\"10.1016/j.acthis.2025.152279\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Prostate cancer (PCa) stands as one of the primary contributors to cancer-related mortality among men globally. It is reported that USP22 functions as an oncogene, while PNMA5 exhibits a significant pro-metastatic effect. This research investigation centered on examining the interplay between USP22 and PNMA5 and their collaborative role in enhancing PCa progression.</p><p><strong>Methods: </strong>The expression of USP22 and PNMA5 in tissue was determined by IHC. The differential expression of cellular USP22 and PNMA5 were detected using qPCR and immunoblotting, respectively. Cell viability and proliferation were assessed by MTT and sphere-formation assay. Transwell and wound-healing assay were conducted to evaluate the metastatic ability. The interaction between USP22 and PNMA5 was detected by Co-IP and IP. A tumor-bearing mice model was established for in vivo detection.</p><p><strong>Results: </strong>USP22 and PNMA5 were highly expressed in both PCa tumor tissues and cells. Knocking down USP22 or PNMA5 inhibited the migration and invasion of PCa cells. USP22 mediated the deubiquitination of PNMA5. PNMA5 overexpression reversed the decrease in cell viability and proliferation rate, as well as the diminished migration and invasion ability induced by USP22 knockdown.</p><p><strong>Conclusion: </strong>USP22 promotes migration and invasion of PCa cells by regulating PNMA5 deubiquitination.</p>\",\"PeriodicalId\":6961,\"journal\":{\"name\":\"Acta histochemica\",\"volume\":\"127 3\",\"pages\":\"152279\"},\"PeriodicalIF\":2.4000,\"publicationDate\":\"2025-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Acta histochemica\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1016/j.acthis.2025.152279\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/8/9 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q4\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta histochemica","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1016/j.acthis.2025.152279","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/8/9 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
USP22-mediated PNMA5 deubiquitination promotes proliferation, migration and invasion of prostate cancer cells.
Background: Prostate cancer (PCa) stands as one of the primary contributors to cancer-related mortality among men globally. It is reported that USP22 functions as an oncogene, while PNMA5 exhibits a significant pro-metastatic effect. This research investigation centered on examining the interplay between USP22 and PNMA5 and their collaborative role in enhancing PCa progression.
Methods: The expression of USP22 and PNMA5 in tissue was determined by IHC. The differential expression of cellular USP22 and PNMA5 were detected using qPCR and immunoblotting, respectively. Cell viability and proliferation were assessed by MTT and sphere-formation assay. Transwell and wound-healing assay were conducted to evaluate the metastatic ability. The interaction between USP22 and PNMA5 was detected by Co-IP and IP. A tumor-bearing mice model was established for in vivo detection.
Results: USP22 and PNMA5 were highly expressed in both PCa tumor tissues and cells. Knocking down USP22 or PNMA5 inhibited the migration and invasion of PCa cells. USP22 mediated the deubiquitination of PNMA5. PNMA5 overexpression reversed the decrease in cell viability and proliferation rate, as well as the diminished migration and invasion ability induced by USP22 knockdown.
Conclusion: USP22 promotes migration and invasion of PCa cells by regulating PNMA5 deubiquitination.
期刊介绍：
Acta histochemica, a journal of structural biochemistry of cells and tissues, publishes original research articles, short communications, reviews, letters to the editor, meeting reports and abstracts of meetings. The aim of the journal is to provide a forum for the cytochemical and histochemical research community in the life sciences, including cell biology, biotechnology, neurobiology, immunobiology, pathology, pharmacology, botany, zoology and environmental and toxicological research. The journal focuses on new developments in cytochemistry and histochemistry and their applications. Manuscripts reporting on studies of living cells and tissues are particularly welcome. Understanding the complexity of cells and tissues, i.e. their biocomplexity and biodiversity, is a major goal of the journal and reports on this topic are especially encouraged. Original research articles, short communications and reviews that report on new developments in cytochemistry and histochemistry are welcomed, especially when molecular biology is combined with the use of advanced microscopical techniques including image analysis and cytometry. Letters to the editor should comment or interpret previously published articles in the journal to trigger scientific discussions. Meeting reports are considered to be very important publications in the journal because they are excellent opportunities to present state-of-the-art overviews of fields in research where the developments are fast and hard to follow. Authors of meeting reports should consult the editors before writing a report. The editorial policy of the editors and the editorial board is rapid publication. Once a manuscript is received by one of the editors, an editorial decision about acceptance, revision or rejection will be taken within a month. It is the aim of the publishers to have a manuscript published within three months after the manuscript has been accepted
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