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长链非编码RNA DHRS4-AS1通过海绵吸附miR-224-3p并上调TP53和TET1来抑制非小细胞肺癌细胞的干性。

LncRNA DHRS4-AS1 Inhibits the Stemness of NSCLC Cells by Sponging miR-224-3p and Upregulating TP53 and TET1.

作者信息

Yan Fei, Zhao Wei, Xu Xiaoyue, Li Chenchen, Li Xiaoyou, Liu Siwen, Shi Lin, Wu Yuan

机构信息

Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, China.

School of Laboratory Medicine/Sichuan Provincial Engineering Laboratory for Prevention and Control Technology of Veterinary Drug Residue in Animal-Origin Food, Chengdu Medical College, Chengdu, China.

出版信息

Front Cell Dev Biol. 2020 Dec 23;8:585251. doi: 10.3389/fcell.2020.585251. eCollection 2020.

DOI:10.3389/fcell.2020.585251
PMID:33425890
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7786137/
Abstract

Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related death. This study aimed to examine the roles of DHRS4-AS1/miR-224-3p signaling in the cancer cell stemness of NSCLC. Real-time PCR showed that DHRS4-AS1 was downregulated in cancerous tissues, and bioinformatics analysis revealed that high DHRS4-AS1 expression indicated a good prognosis for NSCLC patients. Sphere and colony formation assays showed that DHRS4-AS1 overexpression significantly suppressed NSCLC cell colony formation and stem cell-like properties. DHRS4-AS1 also abrogated the expression of OCT4, SOX2, CD34, and CD133, markedly inhibited the expression of epithelial-mesenchymal transition (EMT)-related factors, N-cadherin, ZEB1, and Vimentin, and increased E-cadherin expression in spheres. Furthermore, luciferase reporter assays and real-time PCR analysis demonstrated that DHRS4-AS1 and miR-224-3p were antagonistically repressed in NSCLC cells. RNA immunoprecipitation (RIP) analysis revealed that DHRS4-AS1 interacted with miR-224-3p. DHRS4-AS1 partially reversed the miR-224-3p-decreased TP53 and TET1, resulting in the inhibition of tumor growth . Finally, TP53 and TET1 were antagonistically regulated by DHRS4-AS1 and miR-224-3p in NSCLC cells. In conclusion, TP53- and TET1-associated DHRS4-AS1/miR-224-3p axis is an essential mechanism by which NSCLC modulates cancer cell stemness.

摘要

非小细胞肺癌（NSCLC）是癌症相关死亡的主要原因。本研究旨在探讨DHRS4-AS1/miR-224-3p信号通路在NSCLC癌细胞干性中的作用。实时定量聚合酶链反应（Real-time PCR）显示，癌组织中DHRS4-AS1表达下调，生物信息学分析表明，DHRS4-AS1高表达提示NSCLC患者预后良好。球体形成和集落形成实验表明，DHRS4-AS1过表达显著抑制NSCLC细胞集落形成和干细胞样特性。DHRS4-AS1还消除了OCT4、SOX2、CD34和CD133的表达，显著抑制上皮-间质转化（EMT）相关因子N-钙黏蛋白、ZEB1和波形蛋白的表达，并增加球体中E-钙黏蛋白的表达。此外，荧光素酶报告基因实验和实时定量聚合酶链反应分析表明，DHRS4-AS1和miR-224-3p在NSCLC细胞中相互拮抗。RNA免疫沉淀（RIP）分析显示，DHRS4-AS1与miR-224-3p相互作用。DHRS4-AS1部分逆转了miR-224-3p降低的TP53和TET1水平，从而抑制肿瘤生长。最后，在NSCLC细胞中，DHRS4-AS1和miR-224-3p对TP53和TET1进行拮抗调节。总之，与TP53和TET1相关的DHRS4-AS1/miR-224-3p轴是NSCLC调节癌细胞干性的重要机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa7e/7786137/df80de8cc0e1/fcell-08-585251-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa7e/7786137/f9edc679e867/fcell-08-585251-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa7e/7786137/e11813b359b5/fcell-08-585251-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa7e/7786137/1699e96f41cc/fcell-08-585251-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa7e/7786137/756d129ceed0/fcell-08-585251-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa7e/7786137/7340553effd0/fcell-08-585251-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa7e/7786137/df80de8cc0e1/fcell-08-585251-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa7e/7786137/f9edc679e867/fcell-08-585251-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa7e/7786137/e11813b359b5/fcell-08-585251-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa7e/7786137/1699e96f41cc/fcell-08-585251-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa7e/7786137/756d129ceed0/fcell-08-585251-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa7e/7786137/7340553effd0/fcell-08-585251-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa7e/7786137/df80de8cc0e1/fcell-08-585251-g0006.jpg

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