表观遗传沉默 ZSCAN23 通过激活 Wnt 信号促进胰腺癌生长

IF 4.4 4区医学 Q2 ONCOLOGY Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-01-16 DOI:10.1080/15384047.2024.2302924

Qian Du, Meiying Zhang, Aiai Gao, Tao He, Mingzhou Guo

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引用次数: 0

摘要

胰腺导管腺癌（PDAC）是恶性程度最高的肿瘤。锌指和含 SCAN 结构域蛋白 23（ZSCAN23）是 SCAN 结构域家族的新成员。其表达调控和生物学功能仍有待阐明。本研究探讨了ZSCAN23在PDAC中的表观遗传调控及其功能。在60.21%（171/284）的PDAC中，ZSCAN23被甲基化，其表达受启动子区甲基化调控。ZSCAN23的表达可抑制细胞增殖、集落形成、迁移和侵袭，并诱导细胞凋亡和G1/S期停滞。ZSCAN23抑制了Panc10.05细胞在小鼠体内的异种移植生长。从机理上讲，ZSCAN23通过与胰腺癌细胞中的肌球蛋白重链9（MYH9）相互作用来抑制Wnt信号转导。ZSCAN23在PDAC中经常发生甲基化，可作为一种检测标记物。ZSCAN23 在体外和体内都能抑制 PDAC 细胞的生长。

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Epigenetic silencing ZSCAN23 promotes pancreatic cancer growth by activating Wnt signaling.

Pancreatic ductal adenocarcinoma (PDAC) is the most malignant tumor. Zinc finger and SCAN domain-containing protein 23 (ZSCAN23) is a new member of the SCAN domain family. The expression regulation and biological function remain to be elucidated. In this study, we explored the epigenetic regulation and the function of ZSCAN23 in PDAC. ZSCAN23 was methylated in 60.21% (171/284) of PDAC and its expression was regulated by promoter region methylation. The expression of ZSCAN23 inhibited cell proliferation, colony formation, migration, invasion, and induced apoptosis and G1/S phase arrest. ZSCAN23 suppressed Panc10.05 cell xenograft growth in mice. Mechanistically, ZSCAN23 inhibited Wnt signaling by interacting with myosin heavy chain 9 (MYH9) in pancreatic cancer cells. ZSCAN23 is frequently methylated in PDAC and may serve as a detective marker. ZSCAN23 suppresses PDAC cell growth both in vitro and in vivo.

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来源期刊

Cancer Biology & Therapy 医学-肿瘤学

CiteScore

7.00

自引率

0.00%

发文量

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.