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长链非编码 RNA DSCAM-AS1 通过作为 miR-384 的分子海绵来调节 AKT3 表达，促进结直肠癌的进展。

LncRNA DSCAM-AS1 promotes colorectal cancer progression by acting as a molecular sponge of miR-384 to modulate AKT3 expression.

机构信息

Department of Gastrointestinal Colorectal and Anal Surgery, China-Japan Union Hospital of Jilin University, Changchun 130021, P.R. China.

Department of Anesthesiology, China-Japan Union Hospital of Jilin University, Changchun 130021, P.R. China.

出版信息

Aging (Albany NY). 2020 May 26;12(10):9781-9792. doi: 10.18632/aging.103243.

DOI:10.18632/aging.103243
PMID:32453706
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7288937/
Abstract

Down Syndrome Cell Adhesion Molecule antisense1 (DSCAM-AS1), a novel long non-coding RNA (lncRNA), reportedly contributes to the development and progression of several cancers. There is a lack of information on its biological role and regulatory mechanism with respect to colorectal cancer (CRC). Here, we discovered that the expression of DSCAM-AS1 exhibited a significant upregulation in CRC tissues and cell lines in comparison with the corresponding control. Increased DSCAM-AS1 expression was associated with poor prognosis for those diagnosed with CRC. Loss-of function assay illustrated that knockdown of DSCAM-AS1 resulted in significant inhibition of cell proliferation, invasion and migration , and impaired tumor growth . MicroRNA-384(miR-384) was directly targeted by DSCAM-AS1 in CRC cells, and repression of DSCAM-AS1 inhibited the expression of AKT3, a known target of miR-384 in CRC. In addition, repression of miR-384 or overexpression of AKT3 could partially rescue the inhibitory effect of DSCAM-AS1 knockdown on CRC progression. In summary, DSCAM-AS1 exerted an oncogenic role in CRC by functioning as a competing endogenous RNA of miR-384 to bring about regulation of AKT3 expression. These results implied that DSCAM-AS1 might be a novel therapeutic target for patients suffering from CRC.

摘要

唐氏综合征细胞黏附分子反义 RNA1（DSCAM-AS1）是一种新型的长非编码 RNA（lncRNA），据报道其参与了多种癌症的发生和发展。然而，关于其在结直肠癌（CRC）中的生物学作用和调控机制的信息还很缺乏。在这里，我们发现与相应对照相比，DSCAM-AS1 在 CRC 组织和细胞系中的表达明显上调。DSCAM-AS1 表达增加与 CRC 患者的预后不良相关。功能丧失实验表明，DSCAM-AS1 的敲低导致细胞增殖、侵袭和迁移显著抑制，肿瘤生长受损。miR-384（miR-384）在 CRC 细胞中被 DSCAM-AS1 直接靶向，而 DSCAM-AS1 的抑制抑制了 AKT3 的表达，AKT3 是 miR-384 在 CRC 中的已知靶标。此外，miR-384 的抑制或 AKT3 的过表达可以部分挽救 DSCAM-AS1 敲低对 CRC 进展的抑制作用。总之，DSCAM-AS1 通过作为 miR-384 的竞争性内源性 RNA 发挥致癌作用，从而调节 AKT3 的表达，在 CRC 中发挥致癌作用。这些结果表明，DSCAM-AS1 可能成为 CRC 患者的一种新的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d63/7288937/0cd7c9c122bb/aging-12-103243-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d63/7288937/f53e3184e8c6/aging-12-103243-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d63/7288937/67096e0ca80d/aging-12-103243-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d63/7288937/c06b85804387/aging-12-103243-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d63/7288937/bc02b774d58e/aging-12-103243-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d63/7288937/a8152d9b14a3/aging-12-103243-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d63/7288937/0cd7c9c122bb/aging-12-103243-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d63/7288937/f53e3184e8c6/aging-12-103243-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d63/7288937/67096e0ca80d/aging-12-103243-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d63/7288937/c06b85804387/aging-12-103243-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d63/7288937/bc02b774d58e/aging-12-103243-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d63/7288937/a8152d9b14a3/aging-12-103243-g005.jpg
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