hpv16e6 / e7介导的PiwiL1表达调控诱导宫颈癌细胞的肿瘤发生

IF 6.6 2区 医学 Q1 Medicine Cellular Oncology Pub Date : 2024-06-01 Epub Date: 2023-12-01 DOI:10.1007/s13402-023-00904-8
Midhunaraj Kunnummal, Pooja Sherly Raveendran, Budhaditya Basu, Sheri Vidya Rani, Riya Ann Paul, Krithiga Kuppusamy, Mary Angelin, Joby Issac, Jackson James, Ani V Das
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引用次数: 0

摘要

目的:据报道,PiwiL1在许多癌症中过表达。然而,这些蛋白参与肿瘤发生及其在癌细胞中的调控的分子机制尚不清楚。我们打算了解PiwiL1在肿瘤发生中的作用及其在宫颈细胞中的调节作用。方法:体外和体内研究PiwiL1功能缺失对宫颈癌细胞肿瘤特性的影响。此外,我们还在体外和体内研究了PiwiL1过表达对正常细胞恶性转化的影响。进一步进行RNA-seq和RIP-seq分析,以深入了解PiwiL1在宫颈癌细胞中的直接和间接靶点。结果:在这里,我们报道了PiwiL1不仅过表达,而且在肿瘤诱导和进展中发挥重要作用。CaSki细胞中PiwiL1的缺失导致肿瘤相关特性的降低,而其上调则导致正常HaCaT细胞的恶性转化。我们的研究描述了HPV癌基因E6和E7与PiwiL1之间的新联系。p53和E2F1以上下文依赖的方式直接结合并差异调节PiwiL1启动子。此外,RNA-seq和RIP-RNA-seq表明,PiwiL1在促进宫颈癌细胞转移中具有强烈而直接的作用。结论:我们的研究表明PiwiL1通过诱导肿瘤相关特性和EMT通路在宫颈癌中发挥致癌基因的作用。HPV致癌基因E6/E7可以正向调节PiwiL1,这一发现提示HPV介导宫颈癌肿瘤发生的可能机制。
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HPV16 E6/E7-mediated regulation of PiwiL1 expression induces tumorigenesis in cervical cancer cells.

Purpose: PiwiL1 has been reported to be over-expressed in many cancers. However, the molecular mechanism by which these proteins contribute to tumorigenesis and their regulation in cancer cells is still unclear. We intend to understand the role of PiwiL1 in tumorigenesis and also its regulation in cervical cells.

Methods: We studied the effect of loss of PiwiL1 function on tumor properties of cervical cancer cells in vitro and in vivo. Also we have looked into the effect of PiwiL1 overexpression in the malignant transformation of normal cells both in vitro and in vivo. Further RNA-seq and RIP-seq analyses were done to get insight of the direct and indirect targets of PiwiL1 in the cervical cancer cells.

Results: Here, we report that PiwiL1 is not only over-expressed, but also play a major role in tumor induction and progression. Abolition of PiwiL1 in CaSki cells led to a decrease in the tumor-associated properties, whereas, its upregulation conferred malignant transformation of normal HaCaT cells. Our study delineates a new link between HPV oncogenes, E6 and E7 with PiwiL1. p53 and E2F1 directly bind and differentially regulate PiwiL1 promoter in a context-dependant manner. Further, RNA-seq together with RIP-RNA-seq suggested a strong and direct role for PiwiL1 in promoting metastasis in cervical cancer cells.

Conclusion: Our study demonstrates that PiwiL1 act as an oncogene in cervical cancer by inducing tumor-associated properties and EMT pathway. The finding that HPV oncogenes, E6/E7 can positively regulate PiwiL1 suggests a possible mechanism behind HPV-mediated tumorigenesis in cervical cancer.

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来源期刊
Cellular Oncology
Cellular Oncology Biochemistry, Genetics and Molecular Biology-Cancer Research
CiteScore
10.40
自引率
1.50%
发文量
0
审稿时长
16 weeks
期刊介绍: The Official Journal of the International Society for Cellular Oncology Focuses on translational research Addresses the conversion of cell biology to clinical applications Cellular Oncology publishes scientific contributions from various biomedical and clinical disciplines involved in basic and translational cancer research on the cell and tissue level, technical and bioinformatics developments in this area, and clinical applications. This includes a variety of fields like genome technology, micro-arrays and other high-throughput techniques, genomic instability, SNP, DNA methylation, signaling pathways, DNA organization, (sub)microscopic imaging, proteomics, bioinformatics, functional effects of genomics, drug design and development, molecular diagnostics and targeted cancer therapies, genotype-phenotype interactions. A major goal is to translate the latest developments in these fields from the research laboratory into routine patient management. To this end Cellular Oncology forms a platform of scientific information exchange between molecular biologists and geneticists, technical developers, pathologists, (medical) oncologists and other clinicians involved in the management of cancer patients. In vitro studies are preferentially supported by validations in tumor tissue with clinicopathological associations.
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