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LINC02202/XBP1 轴在黑色素瘤中的转录组学分析:对药物靶向和 PD-1 单克隆抗体疗效的影响。

Transcriptomics analysis of LINC02202/XBP1 axis in melanoma: Implications for drug targeting and PD-1 monoclonal antibody efficacy.

机构信息

School of Public Health, Ningxia Medical University, Yinchuan, China.

Ningxia Medical University, Yinchuan, China.

出版信息

J Cell Mol Med. 2024 Apr;28(8):e18247. doi: 10.1111/jcmm.18247.

DOI:10.1111/jcmm.18247
PMID:38520212
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10960173/
Abstract

Malignant melanoma (MM) is a highly aggressive and deadly form of skin cancer, primarily caused by recurrence and metastasis. Therefore, it is crucial to investigate the regulatory mechanisms underlying melanoma recurrence and metastasis. Our study has identified a potential targeted regulatory relationship between LINC02202, miR-526b-3p and XBP1 in malignant melanoma. Through the regulation of the miR-526b-3p/XBP1 signalling pathway, LINC02202 may play a role in tumour progression and immune infiltration and inhibiting the expression of LINC02202 can increase the efficacy of immunotherapy for melanoma. Our findings shed light on the impact of LINC02202/XBP1 on the phenotype and function of malignant melanoma cells. Furthermore, this study provides a theoretical foundation for the development of novel immunotherapy strategies for malignant melanoma.

摘要

恶性黑色素瘤(MM)是一种高度侵袭性和致命性的皮肤癌,主要由复发和转移引起。因此,研究黑色素瘤复发和转移的调控机制至关重要。我们的研究已经确定了 LINC02202、miR-526b-3p 和 XBP1 在恶性黑色素瘤中潜在的靶向调控关系。通过调节 miR-526b-3p/XBP1 信号通路,LINC02202 可能在肿瘤进展和免疫浸润中发挥作用,抑制 LINC02202 的表达可以提高黑色素瘤免疫治疗的疗效。我们的研究结果揭示了 LINC02202/XBP1 对恶性黑色素瘤细胞表型和功能的影响。此外,本研究为恶性黑色素瘤新型免疫治疗策略的发展提供了理论基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8e1/10960173/20d4ba742067/JCMM-28-e18247-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8e1/10960173/f2fcc4a025bc/JCMM-28-e18247-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8e1/10960173/f676a3628f05/JCMM-28-e18247-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8e1/10960173/9a9d4ba926da/JCMM-28-e18247-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8e1/10960173/8639df87587d/JCMM-28-e18247-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8e1/10960173/bb19ce6a0584/JCMM-28-e18247-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8e1/10960173/56d92d050d48/JCMM-28-e18247-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8e1/10960173/20d4ba742067/JCMM-28-e18247-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8e1/10960173/f2fcc4a025bc/JCMM-28-e18247-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8e1/10960173/f676a3628f05/JCMM-28-e18247-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8e1/10960173/9a9d4ba926da/JCMM-28-e18247-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8e1/10960173/8639df87587d/JCMM-28-e18247-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8e1/10960173/bb19ce6a0584/JCMM-28-e18247-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8e1/10960173/56d92d050d48/JCMM-28-e18247-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8e1/10960173/20d4ba742067/JCMM-28-e18247-g006.jpg

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本文引用的文献

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Secretogranin II influences the assembly and function of MHC class I in melanoma.
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Cancer cell-intrinsic XBP1 drives immunosuppressive reprogramming of intratumoral myeloid cells by promoting cholesterol production.癌细胞内在的XBP1通过促进胆固醇生成来驱动肿瘤内髓样细胞的免疫抑制重编程。
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