新型 miR-3940-5p 靶点 PDLIM1 可调控弥漫大 B 细胞淋巴瘤的恶性进展。

IF 4.4 4区 医学 Q2 ONCOLOGY Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-11-20 DOI:10.1080/15384047.2024.2429175
Jinfeng Zhu, Huifang Xiao, Chuntuan Li, Xiaofeng Li, Jinyang Zheng, Xihu Yao, Shaoxiong Wang, Xiongpeng Zhu
{"title":"新型 miR-3940-5p 靶点 PDLIM1 可调控弥漫大 B 细胞淋巴瘤的恶性进展。","authors":"Jinfeng Zhu, Huifang Xiao, Chuntuan Li, Xiaofeng Li, Jinyang Zheng, Xihu Yao, Shaoxiong Wang, Xiongpeng Zhu","doi":"10.1080/15384047.2024.2429175","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>PDZ And LIM domain protein 1 (PDLIM1), a protein-coding gene, has been widely reported to exhibit differential expression patterns across various human cancers, including hematological malignancies. This study aimed to investigate PDLIM1 expression pattern and its functional role in diffuse large B-cell lymphoma (DLBCL) both <i>in vitro</i> and <i>in vivo</i>.</p><p><strong>Methods: </strong>PDLIM1 expression patterns were reanalyzed using data from the Gene Expression Omnibus, and the results were subsequently validated in patient tissue samples and a panel of four DLBCL cell lines. MicroRNA-3940-5p (miR-3940-5p) was identified as an upstream regulator of PDLIM1. The interaction between PDLIM1 and miR-3940-5p and its effects on DLBCL cellular activities and cancer development were further explored using a DLBCL mouse model.</p><p><strong>Results: </strong>Elevated PDLIM1 expression was observed in DLBCL cells and tissues. Reduced cell proliferation and increased DLBCL cell apoptosis were observed following the knockdown of this gene. Furthermore, short hairpin RNA (shRNA)-mediated PDLIM1 knockdown diminished tumorigenesis of DLBCL cells in nude mice. miR-3940-5p was identified as an upstream regulator of PDLIM1. PDLIM1 expression and function were negatively modulated by the upregulation of miR-3940-5p, consequently affecting the malignant phenotype of DLBCL cells.</p><p><strong>Conclusion: </strong>These findings suggest that the miR-3940-5p/PDLIM1 axis may play a crucial role in DLBCL pathogenesis and could potentially be exploited for therapeutic interventions.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2429175"},"PeriodicalIF":4.4000,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11581179/pdf/","citationCount":"0","resultStr":"{\"title\":\"PDLIM1, a novel miR-3940-5p target, regulates the malignant progression of diffuse large B-cell lymphoma.\",\"authors\":\"Jinfeng Zhu, Huifang Xiao, Chuntuan Li, Xiaofeng Li, Jinyang Zheng, Xihu Yao, Shaoxiong Wang, Xiongpeng Zhu\",\"doi\":\"10.1080/15384047.2024.2429175\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>PDZ And LIM domain protein 1 (PDLIM1), a protein-coding gene, has been widely reported to exhibit differential expression patterns across various human cancers, including hematological malignancies. This study aimed to investigate PDLIM1 expression pattern and its functional role in diffuse large B-cell lymphoma (DLBCL) both <i>in vitro</i> and <i>in vivo</i>.</p><p><strong>Methods: </strong>PDLIM1 expression patterns were reanalyzed using data from the Gene Expression Omnibus, and the results were subsequently validated in patient tissue samples and a panel of four DLBCL cell lines. MicroRNA-3940-5p (miR-3940-5p) was identified as an upstream regulator of PDLIM1. The interaction between PDLIM1 and miR-3940-5p and its effects on DLBCL cellular activities and cancer development were further explored using a DLBCL mouse model.</p><p><strong>Results: </strong>Elevated PDLIM1 expression was observed in DLBCL cells and tissues. Reduced cell proliferation and increased DLBCL cell apoptosis were observed following the knockdown of this gene. Furthermore, short hairpin RNA (shRNA)-mediated PDLIM1 knockdown diminished tumorigenesis of DLBCL cells in nude mice. miR-3940-5p was identified as an upstream regulator of PDLIM1. PDLIM1 expression and function were negatively modulated by the upregulation of miR-3940-5p, consequently affecting the malignant phenotype of DLBCL cells.</p><p><strong>Conclusion: </strong>These findings suggest that the miR-3940-5p/PDLIM1 axis may play a crucial role in DLBCL pathogenesis and could potentially be exploited for therapeutic interventions.</p>\",\"PeriodicalId\":9536,\"journal\":{\"name\":\"Cancer Biology & Therapy\",\"volume\":\"25 1\",\"pages\":\"2429175\"},\"PeriodicalIF\":4.4000,\"publicationDate\":\"2024-12-31\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11581179/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cancer Biology & Therapy\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1080/15384047.2024.2429175\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/11/20 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer Biology & Therapy","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/15384047.2024.2429175","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/11/20 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

背景:PDZ 和 LIM 结构域蛋白 1(PDLIM1)是一种蛋白编码基因,已被广泛报道在包括血液恶性肿瘤在内的各种人类癌症中表现出不同的表达模式。本研究旨在研究 PDLIM1 在弥漫大 B 细胞淋巴瘤(DLBCL)中的体外和体内表达模式及其功能作用:方法:利用基因表达总库(Gene Expression Omnibus)中的数据重新分析了PDLIM1的表达模式,随后在患者组织样本和四种DLBCL细胞系中验证了结果。微RNA-3940-5p(miR-3940-5p)被确定为PDLIM1的上游调节因子。利用DLBCL小鼠模型进一步探讨了PDLIM1和miR-3940-5p之间的相互作用及其对DLBCL细胞活性和癌症发展的影响:结果:在DLBCL细胞和组织中观察到PDLIM1表达升高。结果:在 DLBCL 细胞和组织中观察到 PDLIM1 表达升高,敲除该基因后细胞增殖减少,DLBCL 细胞凋亡增加。此外,短发夹核糖核酸(shRNA)介导的 PDLIM1 基因敲除减少了裸鼠 DLBCL 细胞的肿瘤发生。PDLIM1的表达和功能受miR-3940-5p上调的负调控,从而影响DLBCL细胞的恶性表型:这些研究结果表明,miR-3940-5p/PDLIM1 轴可能在 DLBCL 发病机制中起着关键作用,有可能被用于治疗干预。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
PDLIM1, a novel miR-3940-5p target, regulates the malignant progression of diffuse large B-cell lymphoma.

Background: PDZ And LIM domain protein 1 (PDLIM1), a protein-coding gene, has been widely reported to exhibit differential expression patterns across various human cancers, including hematological malignancies. This study aimed to investigate PDLIM1 expression pattern and its functional role in diffuse large B-cell lymphoma (DLBCL) both in vitro and in vivo.

Methods: PDLIM1 expression patterns were reanalyzed using data from the Gene Expression Omnibus, and the results were subsequently validated in patient tissue samples and a panel of four DLBCL cell lines. MicroRNA-3940-5p (miR-3940-5p) was identified as an upstream regulator of PDLIM1. The interaction between PDLIM1 and miR-3940-5p and its effects on DLBCL cellular activities and cancer development were further explored using a DLBCL mouse model.

Results: Elevated PDLIM1 expression was observed in DLBCL cells and tissues. Reduced cell proliferation and increased DLBCL cell apoptosis were observed following the knockdown of this gene. Furthermore, short hairpin RNA (shRNA)-mediated PDLIM1 knockdown diminished tumorigenesis of DLBCL cells in nude mice. miR-3940-5p was identified as an upstream regulator of PDLIM1. PDLIM1 expression and function were negatively modulated by the upregulation of miR-3940-5p, consequently affecting the malignant phenotype of DLBCL cells.

Conclusion: These findings suggest that the miR-3940-5p/PDLIM1 axis may play a crucial role in DLBCL pathogenesis and could potentially be exploited for therapeutic interventions.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Cancer Biology & Therapy
Cancer Biology & Therapy 医学-肿瘤学
CiteScore
7.00
自引率
0.00%
发文量
60
审稿时长
2.3 months
期刊介绍: Cancer, the second leading cause of death, is a heterogenous group of over 100 diseases. Cancer is characterized by disordered and deregulated cellular and stromal proliferation accompanied by reduced cell death with the ability to survive under stresses of nutrient and growth factor deprivation, hypoxia, and loss of cell-to-cell contacts. At the molecular level, cancer is a genetic disease that develops due to the accumulation of mutations over time in somatic cells. The phenotype includes genomic instability and chromosomal aneuploidy that allows for acceleration of genetic change. Malignant transformation and tumor progression of any cell requires immortalization, loss of checkpoint control, deregulation of growth, and survival. A tremendous amount has been learned about the numerous cellular and molecular genetic changes and the host-tumor interactions that accompany tumor development and progression. It is the goal of the field of Molecular Oncology to use this knowledge to understand cancer pathogenesis and drug action, as well as to develop more effective diagnostic and therapeutic strategies for cancer. This includes preventative strategies as well as approaches to treat metastases. With the availability of the human genome sequence and genomic and proteomic approaches, a wealth of tools and resources are generating even more information. The challenge will be to make biological sense out of the information, to develop appropriate models and hypotheses and to translate information for the clinicians and the benefit of their patients. Cancer Biology & Therapy aims to publish original research on the molecular basis of cancer, including articles with translational relevance to diagnosis or therapy. We will include timely reviews covering the broad scope of the journal. The journal will also publish op-ed pieces and meeting reports of interest. The goal is to foster communication and rapid exchange of information through timely publication of important results using traditional as well as electronic formats. The journal and the outstanding Editorial Board will strive to maintain the highest standards for excellence in all activities to generate a valuable resource.
期刊最新文献
Red ginseng polysaccharide promotes ferroptosis in gastric cancer cells by inhibiting PI3K/Akt pathway through down-regulation of AQP3. Diagnostic value of 18F-PSMA-1007 PET/CT for predicting the pathological grade of prostate cancer. Correction. WYC-209 inhibited GC malignant progression by down-regulating WNT4 through RARα. Efficacy and pharmacodynamic effect of anti-CD73 and anti-PD-L1 monoclonal antibodies in combination with cytotoxic therapy: observations from mouse tumor models.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1