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长链非编码 RNA TPT1-AS1 通过上调 TPT1 介导的 FAK 和 JAK-STAT3 信号通路促进结直肠癌的进展和转移。

Long noncoding RNA TPT1-AS1 promotes the progression and metastasis of colorectal cancer by upregulating the TPT1-mediated FAK and JAK-STAT3 signalling pathways.

机构信息

Department of Minimally Invasive Surgery, The Second Xiangya Hospital of Central South University, Changsha 410011, Hunan, China.

出版信息

Aging (Albany NY). 2021 Jan 10;13(3):3779-3797. doi: 10.18632/aging.202339.

DOI:10.18632/aging.202339
PMID:33428595
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7906141/
Abstract

Tumour protein translationally controlled 1 (TPT1) antisense RNA 1 (TPT1-AS1) is known to be involved in the development and metastasis of cervical and ovarian cancers; however, its biological role in colorectal cancer (CRC) remains unknown. This study aimed to determine the function and mechanism of action of TPT1-AS1 in the progression and metastasis of CRC. Elevated TPT1-AS1 levels were observed in CRC tissues. Furthermore, the high expression levels were found to be correlated with unfavourable clinicopathological characteristics in CRC. Cell function experiments demonstrated that TPT1-AS1 depletion impeded cell proliferation, migration and invasion and enhanced cell adhesion; it also attenuated tumorigenesis and metastasis . Additionally, TPT1-AS1 was predominately located in the nuclei of the cells and could upregulate the expression of TPT1 by recruiting mixed lineage leukaemia protein-1 (MLL1), which increased the trimethylation of H3K4 me3 in the TPT1 promoter region and subsequently activated FAK and JAK-STAT3 signalling cascades. The inhibition of FAK activation by PF573228 significantly attenuated the oncogenic effect of TPT1-AS1. These findings indicated that TPT1-AS1 promoted tumour progression and metastasis in CRC by upregulating TPT1 levels and activating the FAK and JAK-STAT3 signalling pathways. Thus, TPT1-AS1 may be considered as a potential therapeutic target for CRC.

摘要

肿瘤蛋白翻译控制因子 1（TPT1）反义 RNA1（TPT1-AS1）已知参与宫颈癌和卵巢癌的发生和转移；然而，其在结直肠癌（CRC）中的生物学作用尚不清楚。本研究旨在确定 TPT1-AS1 在 CRC 进展和转移中的功能和作用机制。在 CRC 组织中观察到 TPT1-AS1 水平升高。此外，高表达水平与 CRC 的不良临床病理特征相关。细胞功能实验表明，TPT1-AS1 耗竭抑制细胞增殖、迁移和侵袭，增强细胞黏附；它还减弱了肿瘤发生和转移。此外，TPT1-AS1 主要位于细胞的核内，并可通过募集混合谱系白血病蛋白-1（MLL1）上调 TPT1 的表达，从而增加 TPT1 启动子区域 H3K4me3 的三甲基化，进而激活 FAK 和 JAK-STAT3 信号级联。PF573228 抑制 FAK 激活显著减弱了 TPT1-AS1 的致癌作用。这些发现表明，TPT1-AS1 通过上调 TPT1 水平并激活 FAK 和 JAK-STAT3 信号通路促进 CRC 肿瘤的进展和转移。因此，TPT1-AS1 可能被认为是 CRC 的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b108/7906141/c5f9c736c51f/aging-13-202339-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b108/7906141/714515558a3b/aging-13-202339-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b108/7906141/0a288605ef28/aging-13-202339-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b108/7906141/73ab1e30904b/aging-13-202339-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b108/7906141/a9dd699cdee0/aging-13-202339-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b108/7906141/75c121dc3ab6/aging-13-202339-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b108/7906141/71325e89bf91/aging-13-202339-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b108/7906141/c5f9c736c51f/aging-13-202339-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b108/7906141/714515558a3b/aging-13-202339-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b108/7906141/0a288605ef28/aging-13-202339-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b108/7906141/73ab1e30904b/aging-13-202339-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b108/7906141/a9dd699cdee0/aging-13-202339-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b108/7906141/75c121dc3ab6/aging-13-202339-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b108/7906141/71325e89bf91/aging-13-202339-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b108/7906141/c5f9c736c51f/aging-13-202339-g007.jpg

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