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N6-甲基腺苷修饰的 CBX1 通过异染色质形成和 STAT1 激活调控鼻咽癌进展。

N -Methyladenosine-Modified CBX1 Regulates Nasopharyngeal Carcinoma Progression Through Heterochromatin Formation and STAT1 Activation.

机构信息

Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, 651 Dongfeng Road East, Guangzhou, Guangdong, 510060, China.

出版信息

Adv Sci (Weinh). 2022 Dec;9(36):e2205091. doi: 10.1002/advs.202205091. Epub 2022 Oct 30.

DOI:10.1002/advs.202205091
PMID:36310139
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9798977/
Abstract

Epitranscriptomic remodeling such as N -methyladenosine (m A) modification plays a critical role in tumor development. However, little is known about the underlying mechanisms connecting m A modification and nasopharyngeal carcinoma (NPC) progression. Here, CBX1 is identified, a histone methylation regulator, to be significantly upregulated with m A hypomethylation in metastatic NPC tissues. The m A-modified CBX1 mRNA transcript is recognized and destabilized by the m A reader YTHDF3. Furthermore, it is revealed that CBX1 promotes NPC cell migration, invasion, and proliferation through transcriptional repression of MAP7 via H3K9me3-mediated heterochromatin formation. In addition to its oncogenic effect, CBX1 can facilitate immune evasion through IFN-γ-STAT1 signaling-mediated PD-L1 upregulation. Clinically, CBX1 serves as an independent predictor for unfavorable prognosis in NPC patients. The results reveal a crosstalk between epitranscriptomic and epigenetic regulation in NPC progression, and shed light on the functions of CBX1 in tumorigenesis and immunomodulation, which may provide an appealing therapeutic target in NPC.

摘要

表观转录组修饰，如 N -甲基腺苷（m A）修饰，在肿瘤发生中发挥着关键作用。然而，m A 修饰与鼻咽癌（NPC）进展之间的潜在机制仍知之甚少。在这里，鉴定出 CBX1，一种组蛋白甲基化调节剂，在转移性 NPC 组织中与 m A 低甲基化显著上调。m A 修饰的 CBX1 mRNA 转录本被 m A 阅读器 YTHDF3 识别并使其不稳定。此外，研究揭示 CBX1 通过 MAP7 的转录抑制促进 NPC 细胞迁移、侵袭和增殖，通过 H3K9me3 介导的异染色质形成实现。除了致癌作用外，CBX1 还可以通过 IFN-γ-STAT1 信号介导的 PD-L1 上调促进免疫逃逸。临床上，CBX1 是 NPC 患者预后不良的独立预测因子。这些结果揭示了 NPC 进展中表观转录组和表观遗传调控之间的串扰，并阐明了 CBX1 在肿瘤发生和免疫调节中的功能，这可能为 NPC 提供有吸引力的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7206/9798977/3dfddfe5d790/ADVS-9-2205091-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7206/9798977/ef583251fe82/ADVS-9-2205091-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7206/9798977/74edb73f2d15/ADVS-9-2205091-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7206/9798977/0087c2de4f95/ADVS-9-2205091-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7206/9798977/79d7acaf6c15/ADVS-9-2205091-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7206/9798977/161af7f4fca8/ADVS-9-2205091-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7206/9798977/53eb0b845b79/ADVS-9-2205091-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7206/9798977/63dc3f974fbb/ADVS-9-2205091-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7206/9798977/3dfddfe5d790/ADVS-9-2205091-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7206/9798977/ef583251fe82/ADVS-9-2205091-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7206/9798977/74edb73f2d15/ADVS-9-2205091-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7206/9798977/0087c2de4f95/ADVS-9-2205091-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7206/9798977/79d7acaf6c15/ADVS-9-2205091-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7206/9798977/161af7f4fca8/ADVS-9-2205091-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7206/9798977/53eb0b845b79/ADVS-9-2205091-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7206/9798977/63dc3f974fbb/ADVS-9-2205091-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7206/9798977/3dfddfe5d790/ADVS-9-2205091-g008.jpg

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