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长链非编码RNA lnc-SNAPC5-3:4通过直接上调非小细胞肺癌中的miR-224-3p抑制恶性肿瘤。

Long noncoding RNA lnc-SNAPC5-3:4 inhibits malignancy by directly upregulating miR-224-3p in non-small cell lung cancer.

作者信息

Hu Chenxi, Wu Shuo, Sun Wen, Li Jiawen, Hui Kaiyuan, Jiang Xiaodong

机构信息

Department of Oncology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, Lianyungang, 222061, Jiangsu, China.

Department of Oncology, Lianyungang Clinical College of Nanjing Medical University, Lianyungang, 222061, Jiangsu, China.

出版信息

Heliyon. 2024 Jan 13;10(2):e24668. doi: 10.1016/j.heliyon.2024.e24668. eCollection 2024 Jan 30.

DOI:10.1016/j.heliyon.2024.e24668
PMID:38312596
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10835238/
Abstract

The mounting body of evidence demonstrates the growing importance of long noncoding RNAs in the advancement of tumors. This study aimed to investigate the molecular mechanism of lnc-SNAPC5-3:4 in non-small cell lung cancer (NSCLC). We investigated the expression of miR-224-3p and lnc-SNAPC5-3:4 in clinical NSCLC samples and NSCLC cell lines using reverse transcription polymerase chain reaction (RT-PCR). studies, A549 cell growth was estimated using Cell Counting Kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EDU), and flow cytometry assays. studies, NSCLC tumorigenesis was determined using xenograft tumor mouse models, tumor growth was evaluated using antigen Kiel 67 (Ki67) staining, and tumor apoptosis was detected through terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. The relationship between lnc-SNAPC5-3:4 and miR-224-3p was determined by luciferase reporter gene assay. Results indicated that the expression of lnc-SNAPC5-3:4 was observed to be downregulated in NSCLC tissues and cell lines. After overexpression of lnc-SNAPC5-3:4 in cultured A549 cells, proliferation decreased and apoptosis increased. Furthermore, the expression of miR-224-3p was targeted and negatively regulated by lnc-SNAPC5-3:4. The lnc-SNAPC5-3:4 upregulation inhibited cell proliferation and promoted apoptosis, which was partially blocked by miR-224-3p overexpression in A549 cells. In addition, we constructed a subcutaneous inoculation model using BALB/c nude mice, and the results indicated that lnc-SNAPC5-3:4 overexpression restrained the growth of subcutaneous tumors, decreased Ki67 expression levels, and increased apoptosis, as indicated by TUNEL staining in nude mice. However, miR-224-3p transfection resulted in the reversal of the inhibitory effect of lnc-SNAPC5-3:4 on tumor growth. In conclusion, our study revealed that lnc-SNAPC5-3:4 inhibits tumor progression in NSCLC by targeting miR-224-3p. This study provides a potential therapeutic target for inhibiting NSCLC progression.

摘要

越来越多的证据表明长链非编码RNA在肿瘤进展中的重要性日益增加。本研究旨在探讨lnc-SNAPC5-3:4在非小细胞肺癌（NSCLC）中的分子机制。我们使用逆转录聚合酶链反应（RT-PCR）检测了临床NSCLC样本和NSCLC细胞系中miR-224-3p和lnc-SNAPC5-3:4的表达。在研究中，使用细胞计数试剂盒-8（CCK-8）、5-乙炔基-2'-脱氧尿苷（EDU）和流式细胞术检测评估A549细胞的生长。在研究中，使用异种移植肿瘤小鼠模型确定NSCLC的肿瘤发生，使用抗原Kiel 67（Ki67）染色评估肿瘤生长，并通过末端脱氧核苷酸转移酶dUTP缺口末端标记（TUNEL）染色检测肿瘤凋亡。通过荧光素酶报告基因检测确定lnc-SNAPC5-3:4与miR-224-

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3c/10835238/90badcca66ef/gr6.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3c/10835238/ee1c9fa63150/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3c/10835238/90badcca66ef/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3c/10835238/a23f3762eab1/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3c/10835238/e6cbb04f7545/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3c/10835238/970adc8ec98b/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3c/10835238/ee7aaba3ba7c/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3c/10835238/ee1c9fa63150/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3c/10835238/90badcca66ef/gr6.jpg

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