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长链非编码RNA MALAT1通过抑制宫颈肿瘤细胞中miR-124的表达促进宫颈癌增殖。

LncRNA MALAT1 Accelerates Cervical Carcinoma Proliferation by Suppressing miR-124 Expression in Cervical Tumor Cells.

作者信息

Liang Tian, Wang Yuchen, Jiao Yu, Cong Shanshan, Jiang Xinyan, Dong Lina, Zhang Guangmei, Xiao Dan

机构信息

Department of Obstetrics and Gynaecology, The 1st Affiliated Hospital of Harbin Medical University, 150001 Harbin, China.

Department of Psychiatry, Qiqihar Medical University, 161006 Qiqihar, China.

出版信息

J Oncol. 2021 Jun 15;2021:8836078. doi: 10.1155/2021/8836078. eCollection 2021.

DOI:10.1155/2021/8836078
PMID:34221014
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8221887/
Abstract

Emerging studies have clarified the critical role of LncRNA MALAT1 in various pathological progressions. Here, we identified its positive relationship with cervical carcinoma proliferation. Cervical carcinoma has been considered as one of the most malignant tumors among female. Thus, our study was designed to investigate the underlying mechanism of LncRNA MALAT1 on cervical tumor cell proliferation. We observed that miR-124 was the potential target of LncRNA MALAT1 in cervical tumor cell lines (Hela, C-33A, Caski, and SiHa), the expression level of which is negatively correlated with LncRNA MALAT1 in cervical tumor cells, tissues of cervical patients, and mice. Gain- or loss-of-function analyses in cervical tumor cells have further verified the regulatory role of MALAT1 on miR-124. Additionally, the proliferation of cervical carcinoma was inhibited by miR-124 overexpression, whereas it was blocked by LV-MALAT1 transfection. assays, overexpression of miR-124, or knockdown of MALAT1 exhibited beneficial effects on tumor weight, size, and volume, together with elevating the survival rate, tightly related with the progression of cervical cancer. In conclusion, LncRNA MALAT1 disabled the effects of miR-124 as an inhibitory sponge, accelerating the progression of cervical carcinoma.

摘要

新兴研究已阐明长链非编码RNA MALAT1在各种病理进展中的关键作用。在此,我们确定了其与宫颈癌增殖的正相关关系。宫颈癌被认为是女性中最恶性的肿瘤之一。因此,我们的研究旨在探讨长链非编码RNA MALAT1对宫颈肿瘤细胞增殖的潜在机制。我们观察到miR-124是宫颈肿瘤细胞系(Hela、C-33A、Caski和SiHa)中长链非编码RNA MALAT1的潜在靶点,其表达水平与宫颈肿瘤细胞、宫颈癌患者组织及小鼠中的长链非编码RNA MALAT1呈负相关。在宫颈肿瘤细胞中进行的功能获得或缺失分析进一步证实了MALAT1对miR-124的调控作用。此外,miR-124过表达抑制了宫颈癌的增殖,而LV-MALAT1转染则阻断了其增殖。实验表明,miR-124的过表达或MALAT1的敲低对肿瘤重量、大小和体积均有有益影响,同时提高了存活率,这与宫颈癌的进展密切相关。总之,长链非编码RNA MALAT1作为抑制性海绵阻断了miR-124的作用,加速了宫颈癌的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d4/8221887/cfb365dc6da2/JO2021-8836078.006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d4/8221887/f375dc3ab305/JO2021-8836078.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d4/8221887/bcb24370ea12/JO2021-8836078.003.jpg
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