肿瘤细胞治疗研究
英文原题：The roles of LncRNA CARMN in cancers: biomarker potential, therapeutic targeting, and immune response.
The roles of LncRNA CARMN in cancers: biomarker potential, therapeutic targeting, and immune response.
长链非编码RNA（LncRNAs）是基因表达和细胞过程的关键调节因子，对癌症研究具有重要意义。
长链非编码 RNA（LncRNA）是基因表达和细胞过程的关键调控因子，对癌症研究具有重要意义。本综述聚焦于 LncRNA CARMN（心脏停搏与调节性肌细胞核蛋白）在多种癌症中的作用。CARMN 最初因其在心脏组织中的功能而被发现，现已在多种肿瘤类型中显示出表达失调，包括宫颈癌、乳腺癌、结直肠癌和食管癌。其表达改变常与肿瘤进展、转移和患者预后相关，提示其作为生物标志物和治疗靶点的潜力。在宫颈癌中，CARMN 作为肿瘤抑制因子的作用通过其与 miR-92a-3p/BTG2 轴的相互作用以及对 Wnt/β-catenin 信号通路的调控来抑制细胞增殖、迁移和侵袭而得以凸显。在乳腺癌中，CARMN 作为增强子 RNA，通过 DHX9 调控 MMP2，从而影响上皮-间质转化和转移。CARMN 在三阴性乳腺癌中的下调与化疗敏感性增强相关。在结直肠癌中，CARMN 的表达受 m6A 甲基化和突变型 p53 调控，通过 miR-5683 和 FGF2 影响肿瘤生长。最后，在食管癌中，CARMN 的遗传变异影响癌症易感性，某些 SNP 和单倍型与风险增加或降低相关。此外，CARMN 与免疫细胞动态之间的关系凸显了其在癌症免疫监视和治疗中的潜在作用。最后，我们发现 CARMN 可能通过影响 NK 细胞和 T 细胞的募集与活化，以及调节巨噬细胞极化，来调控肿瘤微环境中的免疫细胞耗竭。本综述强调了CARMN在不同癌症中的多样作用及其作为诊断和治疗工具的潜力。未来研究应解决CARMN参与癌症的机制细节，验证其临床实用性，并探索其与现有治疗联合的治疗潜力。
Long non-coding RNAs (LncRNAs) are crucial regulators of gene expression and cellular processes, with significant implications for cancer research. This review focuses on the role of LncRNA CARMN (Cardiac Arrest and Regulated Myocyte Nuclear Protein) in various cancers. CARMN, originally identified for its function in cardiac tissues, has shown dysregulated expression in several tumor types, including cervical, breast, colorectal, and esophageal cancers. Its altered expression often correlates with tumor progression, metastasis, and patient prognosis, suggesting its potential as both a biomarker and therapeutic target. In cervical cancer, CARMN's role as a tumor suppressor is highlighted by its ability to inhibit cell proliferation, migration, and invasion through interaction with the miR-92a-3p/BTG2 axis and modulation of the Wnt/β-catenin signaling pathway. In breast cancer, CARMN acts as an enhancer RNA, affecting epithelial-mesenchymal transition and metastasis by regulating MMP2 via DHX9. The downregulation of CARMN in triple-negative breast cancer is associated with enhanced sensitivity to chemotherapy. In colorectal cancer, CARMN's expression is regulated by m6A methylation and mutant p53, influencing tumor growth through miR-5683 and FGF2. Lastly, in esophageal cancer, genetic variations in CARMN affect cancer susceptibility, with certain SNPs and haplotypes associated with either increased or decreased risk. Additionally, the relationship between CARMN and immune cell dynamics highlights its potential role in cancer immune surveillance and therapy. Finally, we found that CARMN may regulate immune cell exhaustion in the tumor microenvironment by influencing the recruitment and activation of NK cells and T cells, as well as modulating macrophage polarization. This review emphasizes the diverse roles of CARMN across different cancers and its potential as a diagnostic and therapeutic tool. Future research should address the mechanistic details of CARMN's involvement in cancer, validate its clinical utility, and explore its therapeutic potential in combination with existing treatments.
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