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SLCO4A1-AS1 通过调节 miR-4701-5p/NFE2L1 轴激活 WNT 通路促进肺腺癌细胞生长并诱导其耐药。

SLCO4A1-AS1 promotes cell growth and induces resistance in lung adenocarcinoma by modulating miR-4701-5p/NFE2L1 axis to activate WNT pathway.

机构信息

Lanzhou University Second Hospital, Lanzhou University Second Clinical Medical College, Lanzhou, China.

Department of Thoracic Surgery, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, Zhengzhou, China.

出版信息

Cancer Med. 2020 Oct;9(19):7205-7217. doi: 10.1002/cam4.3270. Epub 2020 Aug 6.

DOI:10.1002/cam4.3270
PMID:32762035
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7541149/
Abstract

Long noncoding RNAs (lncRNAs) possessed essential functions in the biological behaviors of various human cancers. SLCO4A1 antisense RNA 1 (SLCO4A1-AS1) is a lncRNA that has been reported as a oncogenic regulator in colorectal cancer and bladder cancer. However, whether it exerted functions in the gene expression and cellular processes in lung adenocarcinoma (LUAD) remains still obscure. In the present research, we unveiled the high level of SLCO4A1-AS1 in LUAD tissues and cells. Moreover, functional assays indicated that SLCO4A-AS1 facilitated LUAD cell proliferation, motility, and cisplatin-resistance. Besides, mechanism investigation revealed that miR-4701-5p could interact with SLCO4A1-AS1 and directly target to NFE2L1. The expression correlation between miR-4701-5p and SLCO4A1-AS1 or NFE2L1 was found to be negative. Moreover, NFE2L1 was expressed at a same tendency with SLCO4A1-AS1 in LUAD tissues and cells. In addition, it was confirmed that NFE2L1 was involved in SLCO4A1-AS1-mediated activation of WNT pathway. According to rescue assays, NFE2L1 could involve in SLCO4A1-AS1-mediated LUAD cell growth. Conclusively, our study demonstrated that SLCO4A1-AS1 facilitated cell growth and enhanced the resistance of LUAD cells to chemotherapy via activating WNT pathway through miR-4701-5p/NFE2L1 axis.

摘要

长链非编码 RNA（lncRNA）在各种人类癌症的生物学行为中具有重要功能。SLCO4A1 反义 RNA 1（SLCO4A1-AS1）是一种 lncRNA，已被报道为结直肠癌和膀胱癌的致癌调节剂。然而，它在肺腺癌（LUAD）中的基因表达和细胞过程中是否发挥作用仍不清楚。在本研究中，我们揭示了 SLCO4A1-AS1 在 LUAD 组织和细胞中的高水平表达。此外，功能分析表明 SLCO4A-AS1 促进 LUAD 细胞增殖、迁移和顺铂耐药性。此外，机制研究表明，miR-4701-5p 可以与 SLCO4A1-AS1 相互作用，并直接靶向 NFE2L1。发现 miR-4701-5p 与 SLCO4A1-AS1 或 NFE2L1 之间的表达相关性呈负相关。此外，在 LUAD 组织和细胞中，NFE2L1 的表达趋势与 SLCO4A1-AS1 相同。此外，还证实 NFE2L1 参与 SLCO4A1-AS1 介导的 WNT 通路激活。根据挽救实验，NFE2L1 可以参与 SLCO4A1-AS1 介导的 LUAD 细胞生长。总之，我们的研究表明，SLCO4A1-AS1 通过 miR-4701-5p/NFE2L1 轴通过激活 WNT 通路促进细胞生长，并增强 LUAD 细胞对化疗的耐药性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2aea/7541149/b923ec558527/CAM4-9-7205-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2aea/7541149/7a01b11c1aec/CAM4-9-7205-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2aea/7541149/cee45ac369ac/CAM4-9-7205-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2aea/7541149/d7eaf4e113cd/CAM4-9-7205-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2aea/7541149/c0e04a0566ac/CAM4-9-7205-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2aea/7541149/2b96e1fed07b/CAM4-9-7205-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2aea/7541149/b923ec558527/CAM4-9-7205-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2aea/7541149/7a01b11c1aec/CAM4-9-7205-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2aea/7541149/cee45ac369ac/CAM4-9-7205-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2aea/7541149/d7eaf4e113cd/CAM4-9-7205-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2aea/7541149/c0e04a0566ac/CAM4-9-7205-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2aea/7541149/2b96e1fed07b/CAM4-9-7205-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2aea/7541149/b923ec558527/CAM4-9-7205-g006.jpg

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