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长链非编码 RNA BMPR1B-AS1 通过海绵吸附 miR-7-2-3p 来调节 DCLK1/Akt/NF-κB 通路,促进子宫内膜癌细胞的增殖和转移。

Long noncoding RNA BMPR1B-AS1 facilitates endometrial cancer cell proliferation and metastasis by sponging miR-7-2-3p to modulate the DCLK1/Akt/NF-κB pathway.

机构信息

Department of Gynecology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou Henan, China.

Academy of Medical Science, Zhengzhou University, Henan, Zhengzhou China.

出版信息

Cell Cycle. 2022 Aug;21(15):1599-1618. doi: 10.1080/15384101.2022.2060003. Epub 2022 Apr 11.

DOI:10.1080/15384101.2022.2060003
PMID:35404759
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9291686/
Abstract

Endometrial carcinoma (EC) originates from the endometrium and is one of the most common tumors in female patients, and its incidence has continued to increase in recent decades. LncRNAs are involved in the pathogenesis and metastasis of a variety of malignant tumors, which indicates that lncRNAs can be used as tumor diagnostic markers and potential therapeutic targets. In this study, we analyzed the RNA transcripts of EC cells from The Cancer Genome Atlas (TCGA) and first reported a novel lncRNA, BMPR1B-AS1, that was more highly expressed in endometrial cancer tissues than in adjacent tissues, and BMPR1B-AS1 could promote endometrial cancer cell proliferation and metastasis. Bioinformatics prediction and experimental results both suggested that BMPR1B-AS1 could modulate the malignant behaviors of endometrial cancer cell lines by sponging miR-7-2-3p to modulate DCLK1, and a DCLK1 inhibitor blocked the activation of the PI3K/Akt/NF-κB signaling pathway. Collectively, this study suggests that the BMPR1B-AS1/miR-7-2-3p/DCLK1 axis contributes to the proliferation and metastasis of endometrial cancer cells via the PI3K/Akt/NF-κB pathway.

摘要

子宫内膜癌(EC)起源于子宫内膜,是女性患者中最常见的肿瘤之一,近年来其发病率持续上升。lncRNAs 参与多种恶性肿瘤的发病机制和转移,表明 lncRNAs 可以作为肿瘤诊断标志物和潜在的治疗靶点。在本研究中,我们分析了来自癌症基因组图谱(TCGA)的 EC 细胞的 RNA 转录物,首次报道了一种新型 lncRNA,BMPR1B-AS1,其在子宫内膜癌组织中的表达高于相邻组织,BMPR1B-AS1 可促进子宫内膜癌细胞的增殖和转移。生物信息学预测和实验结果均表明,BMPR1B-AS1 可以通过海绵 miR-7-2-3p 来调节 DCLK1,从而调节子宫内膜癌细胞系的恶性行为,DCLK1 抑制剂阻断了 PI3K/Akt/NF-κB 信号通路的激活。综上所述,本研究表明,BMPR1B-AS1/miR-7-2-3p/DCLK1 轴通过 PI3K/Akt/NF-κB 通路促进子宫内膜癌细胞的增殖和转移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a9c/9291686/4f71bcf9ea1f/KCCY_A_2060003_F0010_C.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a9c/9291686/eb2483f60bb5/KCCY_A_2060003_F0004_C.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a9c/9291686/8b4ecc86163d/KCCY_A_2060003_F0009_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a9c/9291686/4f71bcf9ea1f/KCCY_A_2060003_F0010_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a9c/9291686/88d11b130a5d/KCCY_A_2060003_F0001_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a9c/9291686/9cc8a610f8e6/KCCY_A_2060003_F0002_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a9c/9291686/634115833d2b/KCCY_A_2060003_F0003_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a9c/9291686/eb2483f60bb5/KCCY_A_2060003_F0004_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a9c/9291686/457efbe2ab5c/KCCY_A_2060003_F0005_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a9c/9291686/3e591eddcaa6/KCCY_A_2060003_F0006_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a9c/9291686/610deac488c3/KCCY_A_2060003_F0007_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a9c/9291686/c156f9d48a0d/KCCY_A_2060003_F0008_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a9c/9291686/8b4ecc86163d/KCCY_A_2060003_F0009_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a9c/9291686/4f71bcf9ea1f/KCCY_A_2060003_F0010_C.jpg

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