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MALAT-1是癌症上皮-间质转化的关键调节因子：一种潜在的转移治疗靶点。

MALAT-1 Is a Key Regulator of Epithelial-Mesenchymal Transition in Cancer: A Potential Therapeutic Target for Metastasis.

作者信息

Hussein Mohamed Ali, Valinezhad Kamyab, Adel Eman, Munirathinam Gnanasekar

机构信息

Department of Pharmaceutical Services, Children's Cancer Hospital Egypt, Cairo 57357, Egypt.

Department of Biology, School of Sciences and Engineering, American University in Cairo, New Cairo 11835, Egypt.

出版信息

Cancers (Basel). 2024 Jan 4;16(1):234. doi: 10.3390/cancers16010234.

DOI:10.3390/cancers16010234
PMID:38201661
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10778055/
Abstract

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.

摘要

转移相关的肺腺癌转录本1（MALAT-1）是一种位于11号染色体q13区域的长链基因间非编码RNA（lncRNA）。它在多种癌症中过度表达，并通过染色质修饰、转录调控和转录后调控来控制基因表达。重要的是，MALAT-1刺激细胞增殖、迁移和转移，并在驱动上皮-间质转化（EMT）中发挥关键作用，随后获得癌症干细胞样特性并产生耐药性。MALAT-1通过与多种细胞内信号通路相互作用来调节EMT，特别是磷酸肌醇3激酶（PI3K）/Akt和Wnt/β-连环蛋白通路。它还像微小RNA的海绵一样，阻止它们与靶基因相互作用并促进EMT。此外，我们使用生物信息学在线工具，利用癌症基因组图谱（TCGA）的数据突出显示正常样本与癌症样本之间MALAT-1表达的差异。此外，MALAT-1与癌症进展和转移的几个关键靶点之间复杂的相互作用使其成为治疗干预的良好候选者。已经开发了几种创新方法来靶向MALAT-1，如短发夹RNA（shRNA）、反义寡核苷酸（ASO）和天然产物。本综述强调了MALAT-1与EMT在调节不同癌症的转移、干性和化疗耐药性方面的相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f35/10778055/0a55a6860832/cancers-16-00234-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f35/10778055/0e4f461f7ee4/cancers-16-00234-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f35/10778055/eafcae43836c/cancers-16-00234-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f35/10778055/b25e8e2e620a/cancers-16-00234-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f35/10778055/0a55a6860832/cancers-16-00234-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f35/10778055/0e4f461f7ee4/cancers-16-00234-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f35/10778055/eafcae43836c/cancers-16-00234-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f35/10778055/b25e8e2e620a/cancers-16-00234-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f35/10778055/0a55a6860832/cancers-16-00234-g004.jpg

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