Metastasis-associated lung adenocarcinoma transcript-1 (MALAT-1) is a long intergenic non-coding RNA (lncRNA) located on chr11q13. It is overexpressed in several cancers and controls gene expression through chromatin modification, transcriptional regulation, and post-transcriptional regulation. Importantly, MALAT-1 stimulates cell proliferation, migration, and metastasis and serves a vital role in driving the epithelial-to-mesenchymal transition (EMT), subsequently acquiring cancer stem cell-like properties and developing drug resistance. MALAT-1 modulates EMT by interacting with various intracellular signaling pathways, notably the phosphoinositide 3-kinase (PI3K)/Akt and Wnt/β-catenin pathways. It also behaves like a sponge for microRNAs, preventing their interaction with target genes and promoting EMT. In addition, we have used bioinformatics online tools to highlight the disparities in the expression of MALAT-1 between normal and cancer samples using data from The Cancer Genome Atlas (TCGA). Furthermore, the intricate interplay of MALAT-1 with several essential targets of cancer progression and metastasis renders it a good candidate for therapeutic interventions. Several innovative approaches have been exploited to target MALAT-1, such as short hairpin RNAs (shRNAs), antisense oligonucleotides (ASOs), and natural products. This review emphasizes the interplay between MALAT-1 and EMT in modulating cancer metastasis, stemness, and chemoresistance in different cancers.
转移相关肺腺癌转录本-1（MALAT-1）是位于染色体11q13区域的长链基因间非编码RNA（lncRNA）。该分子在多种癌症中过度表达，并通过染色质修饰、转录调控及转录后调控机制影响基因表达。值得注意的是，MALAT-1能够促进细胞增殖、迁移和转移，在上皮-间质转化（EMT）过程中发挥关键作用，进而使细胞获得类癌症干细胞特性并产生耐药性。MALAT-1通过调控多种细胞内信号通路（尤其是磷脂酰肌醇3-激酶（PI3K）/Akt和Wnt/β-连环蛋白通路）来调节EMT进程。同时它还能作为微小RNA的分子海绵，阻断其与靶基因的结合从而促进EMT。此外，我们利用生物信息学在线工具，基于癌症基因组图谱（TCGA）数据揭示了MALAT-1在正常样本与癌症样本中的表达差异。MALAT-1与癌症进展及转移关键靶点之间复杂的相互作用网络，使其成为极具潜力的治疗干预靶点。目前已有多种靶向MALAT-1的创新策略被开发，包括短发夹RNA（shRNA）、反义寡核苷酸（ASO）及天然产物等。本综述重点阐述MALAT-1与EMT在不同癌症转移、干细胞特性及化疗耐药调控中的相互作用机制。
肿瘤(癌症)患者之家