γ-丁甜菜碱羟化酶1反义RNA 1在癌发生和肿瘤进展中的作用综述。
A review on the role of gamma-butyrobetaine hydroxylase 1 antisense RNA 1 in the carcinogenesis and tumor progression.
发表日期:2023 Nov 05
作者:
Juan Hu, Jipeng Liu, Siwei Zhou, Hongliang Luo
来源:
Cell Death & Disease
摘要:
γ-丁酰甜菜碱羟化酶 1 反义 RNA 1 (BBOX1-AS1) 位于人类染色体 11 p14 上,在肿瘤发生中发挥着关键作用,具有多种致癌作用。 BBOX1-AS1 的异常表达复杂地调节各种细胞过程,包括细胞生长、上皮间质转化、迁移、侵袭、转移、细胞死亡和干性。值得注意的是,BBOX1-AS1的表达与临床病理特征和肿瘤预后显着相关,也可用于肺癌和食管癌的诊断。通过参与 ceRNA 网络,BBOX1-AS1 竞争性地结合 10 种不同癌症类型中的 8 种 miRNA。此外,BBOX1-AS1 可以直接调节下游蛋白质编码基因或充当 mRNA 稳定剂。 BBOX1-AS1 的影响延伸至关键信号通路,包括 Hedgehog、Wnt/β-catenin 和 MELK/FAK 通路。此外,它还影响肝细胞癌的耐药性。本研究对 BBOX1-AS1 在不同肿瘤类型中异常表达的临床意义进行了系统评价。它揭示了 BBOX1-AS1 影响癌症发生和进展的复杂分子机制,并概述了该领域未来研究的潜在途径。© 2023。作者。
Gamma-butyrobetaine hydroxylase 1 antisense RNA 1 (BBOX1-AS1), located on human chromosome 11 p14, emerges as a critical player in tumorigenesis with diverse oncogenic effects. Aberrant expression of BBOX1-AS1 intricately regulates various cellular processes, including cell growth, epithelial-mesenchymal transition, migration, invasion, metastasis, cell death, and stemness. Notably, the expression of BBOX1-AS1 was significantly correlated with clinical-pathological characteristics and tumor prognoses, and it could also be used for the diagnosis of lung and esophageal cancers. Through its involvement in the ceRNA network, BBOX1-AS1 competitively binds to eight miRNAs in ten different cancer types. Additionally, BBOX1-AS1 can directly modulate downstream protein-coding genes or act as an mRNA stabilizer. The implications of BBOX1-AS1 extend to critical signaling pathways, including Hedgehog, Wnt/β-catenin, and MELK/FAK pathways. Moreover, it influences drug resistance in hepatocellular carcinoma. The present study provides a systematic review of the clinical significance of BBOX1-AS1's aberrant expression in diverse tumor types. It sheds light on the intricate molecular mechanisms through which BBOX1-AS1 influences cancer initiation and progression and outlines potential avenues for future research in this field.© 2023. The Author(s).