敲除 CPSF4 可通过上调 NRF1 抑制膀胱癌细胞生长

IF 2.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Biochemical Genetics Pub Date : 2024-07-22 DOI:10.1007/s10528-024-10891-6
Yixiang Sun, Guanglei Li, Hanlin Zhang, Mao Xie
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引用次数: 0

摘要

越来越多的研究表明,核呼吸因子1(NRF1)缺乏经常发生在许多人类疾病中,而激活NRF1可以保护神经元和其他细胞免受退行性疾病和恶性肿瘤的侵袭。然而,NRF1在膀胱癌中如何调控仍是未知数。我们的研究旨在揭示叶绿素和多腺苷酸化特异性因子4(CPSF4)对膀胱癌生长抑制作用的作用,并阐明其与NRF1的关系。本研究采用细胞增殖试验、Transwell迁移试验和多细胞肿瘤球(MCTS)形成试验来检测膀胱癌细胞系中肿瘤细胞的生长情况。通过 Western bolt 检测确定了 NRF1 和 CPSF4 之间的关系。此外,为了进一步验证 CPSF4 对膀胱肿瘤的抑制作用以及对 NRF1 的调控作用,还建立了裸鼠皮下异种移植肿瘤。体外实验结果表明,敲除CPSF4能显著降低5637和HT1376细胞株的增殖和迁移,抑制MCTS的形成,而额外敲除CPSF4引起的NRF1增高则能部分消除这些效应。体内研究结果表明,CPSF4的敲除可显著减少皮下肿瘤的体积和重量,并降低肿瘤组织中Ki-67的表达,而NRF1的敲除可部分逆转CPSF4敲除所诱导的这些效应。Western bolt实验表明,CPSF4能负向调节NRF1。我们的研究结果表明,敲除CPSF4可通过上调NRF1抑制膀胱癌细胞的生长,这可能为CPSF4作为膀胱癌的治疗靶点提供了证据。
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Knockdown of CPSF4 Inhibits Bladder Cancer Cell Growth by Upregulating NRF1.

Increasing studies have shown that nuclear respiratory factor 1 (NRF1) deficiency frequently occurs in many human diseases, and its activation can protect neurons and other cells from degenerative diseases and malignant tumors. However, how NRF1 is regulated in bladder cancer remains unknown. Our research aims to reveal the role of leavage and polyadenylation-specific factor 4 (CPSF4) on the growth inhibition effect of bladder cancer and clarify its relationship with NRF1. Here, cell proliferation assay, transwell migration assay and multicellular tumor spheroids (MCTS) formation assay in the bladder cancer cell lines were carried out to measure tumor cell growth. Western bolt assay was carried out to identify the relationship between NRF1 and CPSF4. Also, subcutaneous xenograft tumors in nude mice were established to further validate the inhibition effect of CPSF4 on bladder tumor and the regulation on NRF1. The results in vitro showed that knockdown of CPSF4 strongly reduced the proliferation and migration, and inhibited MCTS formation in 5637 and HT1376 cell lines, while an additional knockdown of increased NRF1 induced by CPSF4 knockdown partially abolished these effects. The results in vivo showed that knockdown of CPSF4 strongly reduced the volume and weight of subcutaneous tumor, and decreased the expression of Ki-67 in tumor tissue, while NRF1 knockdown partially reversed these effects induced by CPSF4 knockdown. Western bolt assay demonstrated that CPSF4 could negatively regulate NRF1. Our results indicated that knock-down of CPSF4 inhibited bladder cancer cell growth by upregulating NRF1, which might provide evidence of CPSF4 as a therapeutic target for bladder cancer.

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来源期刊
Biochemical Genetics
Biochemical Genetics 生物-生化与分子生物学
CiteScore
3.90
自引率
0.00%
发文量
133
审稿时长
4.8 months
期刊介绍: Biochemical Genetics welcomes original manuscripts that address and test clear scientific hypotheses, are directed to a broad scientific audience, and clearly contribute to the advancement of the field through the use of sound sampling or experimental design, reliable analytical methodologies and robust statistical analyses. Although studies focusing on particular regions and target organisms are welcome, it is not the journal’s goal to publish essentially descriptive studies that provide results with narrow applicability, or are based on very small samples or pseudoreplication. Rather, Biochemical Genetics welcomes review articles that go beyond summarizing previous publications and create added value through the systematic analysis and critique of the current state of knowledge or by conducting meta-analyses. Methodological articles are also within the scope of Biological Genetics, particularly when new laboratory techniques or computational approaches are fully described and thoroughly compared with the existing benchmark methods. Biochemical Genetics welcomes articles on the following topics: Genomics; Proteomics; Population genetics; Phylogenetics; Metagenomics; Microbial genetics; Genetics and evolution of wild and cultivated plants; Animal genetics and evolution; Human genetics and evolution; Genetic disorders; Genetic markers of diseases; Gene technology and therapy; Experimental and analytical methods; Statistical and computational methods.
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