Yuting Guo, She Tian, Haiyang Li, Shi Zuo, Chao Yu, Chengyi Sun
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The binding of KLF9 to the KIAA1522 promoter was analyzed by dual-luciferase assay and chromatin immunoprecipitation. The rescue experiment was conducted to analyze the role of KIAA1522.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>KLF9 was downregulated, while KIAA1522 was upregulated in PC cells. KLF9 overexpression mitigated the proliferation, invasion, and migration of PC cells. Enrichment of KLF9 led to inhibition of the KIAA1522 promoter and repressed KIAA1522 expression. KIAA1522 overexpression neutralized the inhibitory role of KLF9 in PC cell functions.</p>\n </section>\n \n <section>\n \n <h3> Conclusion</h3>\n \n <p>KLF9 is enriched in the KIAA1522 promoter and negatively regulates KIAA1522 expression, thereby mitigating the proliferation, invasion, and migration of PC cells.</p>\n </section>\n </div>","PeriodicalId":8633,"journal":{"name":"Asia-Pacific journal of clinical oncology","volume":null,"pages":null},"PeriodicalIF":1.4000,"publicationDate":"2024-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Transcription factor KLF9 inhibits the proliferation, invasion, and migration of pancreatic cancer cells by repressing KIAA1522\",\"authors\":\"Yuting Guo, She Tian, Haiyang Li, Shi Zuo, Chao Yu, Chengyi Sun\",\"doi\":\"10.1111/ajco.14048\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n \\n <section>\\n \\n <h3> Aim</h3>\\n \\n <p>Pancreatic cancer (PC) has a poor prognosis and high mortality. 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引用次数: 0
摘要
目的：胰腺癌（PC）预后差，死亡率高。Kruppel 样因子 9（KLF9）是一种转录因子，在多种肿瘤中异常表达。本研究试图分析 KLF9 在 PC 细胞增殖、侵袭和迁移中的功能作用：方法：采用实时定量聚合酶链反应和 Western 印迹检测法测定 KLF9 和 KIAA1522 在正常胰腺细胞（HPDE-C7）和 PC 细胞（Panc 03.27、BxPc3、SW1990）中的表达模式。细胞计数试剂盒-8、5-乙炔基-2'-脱氧尿苷染色和 Transwell 试验评估了 KLF9 过表达处理后的细胞增殖、侵袭和迁移情况。通过双荧光素酶检测和染色质免疫沉淀分析了 KLF9 与 KIAA1522 启动子的结合。实验结果表明，KLF9与KIAA1522启动子的结合被下调：结果：PC细胞中KLF9下调，而KIAA1522上调。KLF9的过表达减轻了PC细胞的增殖、侵袭和迁移。KLF9 的富集会抑制 KIAA1522 启动子，并抑制 KIAA1522 的表达。KIAA1522的过表达中和了KLF9在PC细胞功能中的抑制作用：结论：KLF9富集于KIAA1522启动子，负向调节KIAA1522的表达，从而减轻PC细胞的增殖、侵袭和迁移。
Transcription factor KLF9 inhibits the proliferation, invasion, and migration of pancreatic cancer cells by repressing KIAA1522
Aim
Pancreatic cancer (PC) has a poor prognosis and high mortality. Kruppel-like factor 9 (KLF9), a transcription factor, is aberrantly expressed in various neoplasms. The current study sought to analyze the functional role of KLF9 in the proliferation, invasion, and migration of PC cells.
Methods
The expression patterns of KLF9 and KIAA1522 in normal pancreatic cells (HPDE-C7) and PC cells (Panc 03.27, BxPc3, SW1990) were determined by real-time quantitative polymerase chain reaction and Western blot assay. After treatment of KLF9 overexpression, proliferation, invasion, and migration were evaluated by cell counting kit-8, 5-ethynyl-2′-deoxyuridine staining, and Transwell assays. The binding of KLF9 to the KIAA1522 promoter was analyzed by dual-luciferase assay and chromatin immunoprecipitation. The rescue experiment was conducted to analyze the role of KIAA1522.
Results
KLF9 was downregulated, while KIAA1522 was upregulated in PC cells. KLF9 overexpression mitigated the proliferation, invasion, and migration of PC cells. Enrichment of KLF9 led to inhibition of the KIAA1522 promoter and repressed KIAA1522 expression. KIAA1522 overexpression neutralized the inhibitory role of KLF9 in PC cell functions.
Conclusion
KLF9 is enriched in the KIAA1522 promoter and negatively regulates KIAA1522 expression, thereby mitigating the proliferation, invasion, and migration of PC cells.
期刊介绍：
Asia–Pacific Journal of Clinical Oncology is a multidisciplinary journal of oncology that aims to be a forum for facilitating collaboration and exchanging information on what is happening in different countries of the Asia–Pacific region in relation to cancer treatment and care. The Journal is ideally positioned to receive publications that deal with diversity in cancer behavior, management and outcome related to ethnic, cultural, economic and other differences between populations. In addition to original articles, the Journal publishes reviews, editorials, letters to the Editor and short communications. Case reports are generally not considered for publication, only exceptional papers in which Editors find extraordinary oncological value may be considered for review. The Journal encourages clinical studies, particularly prospectively designed clinical trials.
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