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Molecular Interactions of the Long Noncoding RNA NEAT1 in Cancer

SIMPLE SUMMARY: In this review, we present current knowledge of LncRNA NEAT1 in the development of malignant diseases. First, we illustrate the structure and functions of NEAT1 in cancer. Then we explore the interaction between NEAT1 and other molecules and analyze the impact of this interaction on...

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Detalles Bibliográficos
Autores principales: Gu, Jingtao, Zhang, Bo, An, Rui, Qian, Weikun, Han, Liang, Duan, Wanxing, Wang, Zheng, Ma, Qingyong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9406559/
https://www.ncbi.nlm.nih.gov/pubmed/36011001
http://dx.doi.org/10.3390/cancers14164009
Descripción
Sumario:SIMPLE SUMMARY: In this review, we present current knowledge of LncRNA NEAT1 in the development of malignant diseases. First, we illustrate the structure and functions of NEAT1 in cancer. Then we explore the interaction between NEAT1 and other molecules and analyze the impact of this interaction on cancer progression. Finally, we summarize the regulation of NEAT1 and the function of NEAT1-containing exosomes. Elucidating the molecular interaction of NEAT1 may shed light on future treatment of cancer. ABSTRACT: As one of the best-studied long noncoding RNAs, nuclear paraspeckle assembly transcript 1 (NEAT1) plays a pivotal role in the progression of cancers. NEAT1, especially its isoform NEAT1-1, facilitates the growth and metastasis of various cancers, excluding acute promyelocytic leukemia. NEAT1 can be elevated via transcriptional activation or stability alteration in cancers changing the aggressive phenotype of cancer cells. NEAT1 can also be secreted from other cells and be delivered to cancer cells through exosomes. Hence, elucidating the molecular interaction of NEAT1 may shed light on the future treatment of cancer. Herein, we review the molecular function of NEAT1 in cancer progression, and explain how NEAT1 interacts with RNAs, proteins, and DNA promoter regions to upregulate tumorigenic factors.