{"title":"UPF1通过调节无义介导的BMP6和lncRNA WAKMAR2的衰变来抑制宫颈癌细胞的迁移和侵袭。","authors":"Guligeina Abudourexiti, Jingjing Zhang, Guzhanuer Abuduxikuer","doi":"10.3802/jgo.2025.36.e127","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>Up-frameshift protein 1 (UPF1) can contribute to the progression of a variety of cancers. Currently, there is limited research on UPF1 in cervical cancer, and further investigation is necessary to understand its regulatory mechanisms in cervical cancer.</p><p><strong>Methods: </strong>mRNA expression was detected by quantitative real-time polymerase chain reaction, while protein expression was quantified by western blotting assay. Cell function was assessed by cell counting kit-8 assay, Transwell assay and wound-healing assay. A xenograft mouse model assay was performed to analyze the effect of UPF1 silencing on tumor formation. Differentially expressed genes in cell samples were screened using the R Bioconductor package DESeq2. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analysis was performed to determine the functional categories of the differentially expressed genes.</p><p><strong>Results: </strong>UPF1 expression was downregulated in cervical cancer tissues and cells. Additionally, UPF1 silencing promoted invasion and migration of cervical cancer cells and tumor formation. There were a total of 188 upregulated genes in the SiHa cells after UPF1 silencing. Biological analysis showed that these upregulated genes were enriched in pathways related to regulation of cell proliferation, positive regulation of gene expression, cell adhesion, and Hippo signaling pathway. Additionally, UPF1 depletion promoted SiHa cell proliferation, invasion and migration, whereas the effects were attenuated after silencing of bone morphogenetic protein 6 (<i>BMP6</i>) or long non-coding RNA (lncRNA) <i>WAKMAR2</i>.</p><p><strong>Conclusion: </strong>UPF1 inhibited cervical cancer cell migration and invasion through the regulation of nonsense-mediated decay of <i>BMP6</i> and lncRNA <i>WAKMAR2</i>.</p>","PeriodicalId":15868,"journal":{"name":"Journal of Gynecologic Oncology","volume":" ","pages":""},"PeriodicalIF":3.7000,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"UPF1 inhibits cervical cancer cell migration and invasion by regulating nonsense-mediated decay of <i>BMP6</i> and lncRNA <i>WAKMAR2</i>.\",\"authors\":\"Guligeina Abudourexiti, Jingjing Zhang, Guzhanuer Abuduxikuer\",\"doi\":\"10.3802/jgo.2025.36.e127\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>Up-frameshift protein 1 (UPF1) can contribute to the progression of a variety of cancers. Currently, there is limited research on UPF1 in cervical cancer, and further investigation is necessary to understand its regulatory mechanisms in cervical cancer.</p><p><strong>Methods: </strong>mRNA expression was detected by quantitative real-time polymerase chain reaction, while protein expression was quantified by western blotting assay. Cell function was assessed by cell counting kit-8 assay, Transwell assay and wound-healing assay. A xenograft mouse model assay was performed to analyze the effect of UPF1 silencing on tumor formation. Differentially expressed genes in cell samples were screened using the R Bioconductor package DESeq2. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analysis was performed to determine the functional categories of the differentially expressed genes.</p><p><strong>Results: </strong>UPF1 expression was downregulated in cervical cancer tissues and cells. Additionally, UPF1 silencing promoted invasion and migration of cervical cancer cells and tumor formation. There were a total of 188 upregulated genes in the SiHa cells after UPF1 silencing. Biological analysis showed that these upregulated genes were enriched in pathways related to regulation of cell proliferation, positive regulation of gene expression, cell adhesion, and Hippo signaling pathway. Additionally, UPF1 depletion promoted SiHa cell proliferation, invasion and migration, whereas the effects were attenuated after silencing of bone morphogenetic protein 6 (<i>BMP6</i>) or long non-coding RNA (lncRNA) <i>WAKMAR2</i>.</p><p><strong>Conclusion: </strong>UPF1 inhibited cervical cancer cell migration and invasion through the regulation of nonsense-mediated decay of <i>BMP6</i> and lncRNA <i>WAKMAR2</i>.</p>\",\"PeriodicalId\":15868,\"journal\":{\"name\":\"Journal of Gynecologic Oncology\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":3.7000,\"publicationDate\":\"2025-06-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Gynecologic Oncology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.3802/jgo.2025.36.e127\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"OBSTETRICS & GYNECOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Gynecologic Oncology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3802/jgo.2025.36.e127","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"OBSTETRICS & GYNECOLOGY","Score":null,"Total":0}
UPF1 inhibits cervical cancer cell migration and invasion by regulating nonsense-mediated decay of BMP6 and lncRNA WAKMAR2.
Objective: Up-frameshift protein 1 (UPF1) can contribute to the progression of a variety of cancers. Currently, there is limited research on UPF1 in cervical cancer, and further investigation is necessary to understand its regulatory mechanisms in cervical cancer.
Methods: mRNA expression was detected by quantitative real-time polymerase chain reaction, while protein expression was quantified by western blotting assay. Cell function was assessed by cell counting kit-8 assay, Transwell assay and wound-healing assay. A xenograft mouse model assay was performed to analyze the effect of UPF1 silencing on tumor formation. Differentially expressed genes in cell samples were screened using the R Bioconductor package DESeq2. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analysis was performed to determine the functional categories of the differentially expressed genes.
Results: UPF1 expression was downregulated in cervical cancer tissues and cells. Additionally, UPF1 silencing promoted invasion and migration of cervical cancer cells and tumor formation. There were a total of 188 upregulated genes in the SiHa cells after UPF1 silencing. Biological analysis showed that these upregulated genes were enriched in pathways related to regulation of cell proliferation, positive regulation of gene expression, cell adhesion, and Hippo signaling pathway. Additionally, UPF1 depletion promoted SiHa cell proliferation, invasion and migration, whereas the effects were attenuated after silencing of bone morphogenetic protein 6 (BMP6) or long non-coding RNA (lncRNA) WAKMAR2.
Conclusion: UPF1 inhibited cervical cancer cell migration and invasion through the regulation of nonsense-mediated decay of BMP6 and lncRNA WAKMAR2.
期刊介绍：
The Journal of Gynecologic Oncology (JGO) is an official publication of the Asian Society of Gynecologic Oncology. Abbreviated title is ''J Gynecol Oncol''. It was launched in 1990. The JGO''s aim is to publish the highest quality manuscripts dedicated to the advancement of care of the patients with gynecologic cancer. It is an international peer-reviewed periodical journal that is published bimonthly (January, March, May, July, September, and November). Supplement numbers are at times published. The journal publishes editorials, original and review articles, correspondence, book review, etc.
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