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JNK 和 p38 MAPK 信号通路在鼻咽癌中的功能作用。

Functional Roles of JNK and p38 MAPK Signaling in Nasopharyngeal Carcinoma.

机构信息

School of Postgraduate Studies, International Medical University, Bukit Jalil, Kuala Lumpur 57000, Malaysia.

Center for Cancer and Stem Cell Research, Development and Innovation (IRDI), Institute for Research, International Medical University, Bukit Jalil, Kuala Lumpur 57000, Malaysia.

出版信息

Int J Mol Sci. 2022 Jan 20;23(3):1108. doi: 10.3390/ijms23031108.

DOI:10.3390/ijms23031108
PMID:35163030
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8834850/
Abstract

c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) family members integrate signals that affect proliferation, differentiation, survival, and migration in a cell context- and cell type-specific way. JNK and p38 MAPK activities are found upregulated in nasopharyngeal carcinoma (NPC). Studies have shown that activation of JNK and p38 MAPK signaling can promote NPC oncogenesis by mechanisms within the cancer cells and interactions with the tumor microenvironment. They regulate multiple transcription activities and contribute to tumor-promoting processes, ranging from cell proliferation to apoptosis, inflammation, metastasis, and angiogenesis. Current literature suggests that JNK and p38 MAPK activation may exert pro-tumorigenic functions in NPC, though the underlying mechanisms are not well documented and have yet to be fully explored. Here, we aim to provide a narrative review of JNK and p38 MAPK pathways in human cancers with a primary focus on NPC. We also discuss the potential therapeutic agents that could be used to target JNK and p38 MAPK signaling in NPC, along with perspectives for future works. We aim to inspire future studies further delineating JNK and p38 MAPK signaling in NPC oncogenesis which might offer important insights for better strategies in diagnosis, prognosis, and treatment decision-making in NPC patients.

摘要

c-Jun N-末端激酶(JNK)和 p38 丝裂原活化蛋白激酶(MAPK)家族成员以细胞上下文和细胞类型特异性的方式整合影响细胞增殖、分化、存活和迁移的信号。JNK 和 p38 MAPK 活性在鼻咽癌(NPC)中上调。研究表明,JNK 和 p38 MAPK 信号的激活可以通过癌细胞内的机制以及与肿瘤微环境的相互作用来促进 NPC 的致癌作用。它们调节多种转录活性,并有助于促进肿瘤的过程,从细胞增殖到细胞凋亡、炎症、转移和血管生成。目前的文献表明,JNK 和 p38 MAPK 的激活可能在 NPC 中发挥促肿瘤作用,但潜在的机制尚未得到很好的记录,也尚未得到充分探索。在这里,我们旨在对人类癌症中的 JNK 和 p38 MAPK 通路进行叙述性综述,重点是 NPC。我们还讨论了可能用于靶向 NPC 中 JNK 和 p38 MAPK 信号的潜在治疗剂,以及未来工作的展望。我们旨在激发未来的研究进一步阐明 NPC 致癌作用中的 JNK 和 p38 MAPK 信号,这可能为 NPC 患者的诊断、预后和治疗决策提供重要的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0eb/8834850/0f613d4f8645/ijms-23-01108-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0eb/8834850/841a11031782/ijms-23-01108-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0eb/8834850/06e0597356aa/ijms-23-01108-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0eb/8834850/0f613d4f8645/ijms-23-01108-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0eb/8834850/841a11031782/ijms-23-01108-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0eb/8834850/06e0597356aa/ijms-23-01108-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0eb/8834850/0f613d4f8645/ijms-23-01108-g003.jpg

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