| 石 悦,谭招丽,张耀月.长链非编码RNA PCED1B-AS1靶向miR-383-5p调控结直肠癌进展的作用分析[J].肿瘤学杂志,2023,29(8):665-672. |
| 长链非编码RNA PCED1B-AS1靶向miR-383-5p调控结直肠癌进展的作用分析 |
| LncRNA PCED1B-AS1 Regulates Colorectal Cancer Progression Through Targeting miR-383-5p |
| 投稿时间：2023-01-30 |
| DOI：10.11735/j.issn.1671-170X.2023.08.B006 |
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| 中文关键词: 结直肠癌 PCED1B-AS1 miR-383-5p 增殖 迁移 凋亡 |
| 英文关键词:colorectal cancer PCED1B-AS1 miR-383-5p proliferation migration apoptosis |
| 基金项目:国家自然科学基金（82002474） |
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| 中文摘要: |
| 摘 要：［目的］ 探讨长链非编码RNA（long non-coding RNA，lncRNA）PCED1B-AS1靶向miR-383-5p在结直肠癌（colorectal cancer，CRC）进展中的作用。［方法］ 收集解放军总医院第五医学中心南院区2018年1月至2019年10月收治的41例CRC组织和癌旁组织，RT-qPCR检测PCED1B-AS1、miR-383-5p和过氧化物酶3（PRDX3）mRNA表达水平。将si-NC、si-PCED1B-AS1、miR-NC、miR-383-5p、si-PCED1B-AS1+anti-miR-NC、si-PCED1B-AS1+anti-miR-383-5p分别转染CRC细胞LoVo，CCK-8法、平板克隆实验、Transwell实验、流式细胞术分别检测LoVo细胞体外增殖、克隆形成、迁移和凋亡能力。双荧光素酶报告实验确定PCED1B-AS1与miR-383-5p、miR-383-5p与PRDX3的靶向关系。［结果］ 与癌旁组织比较，CRC组织中PCED1B-AS1（0.92±0.12 vs 2.87±0.32）、PRDX3 mRNA（0.93±0.11 vs 2.30±0.26）表达水平升高（P均<0.001），miR-383-5p表达水平降低（0.98±0.15 vs 0.40±0.05，P<0.001）。下调PCED1B-AS1后LoVo细胞miR-383-5p表达水平（1.00±0.00 vs 2.95±0.12）、抑制率（0 vs 47.75%±2.75%）、凋亡率均升高（8.10%±0.75% vs 20.20%±1.09%）（P均<0.001），PRDX3 mRNA表达水平（1.00±0.00 vs 0.27±0.03）、克隆形成数（116.78±6.01 vs 67.56±4.11）、迁移细胞数（173.78±8.32 vs 85.89±3.07）均降低（P均<0.001）。过表达miR-383-5p后LoVo细胞PRDX3 mRNA表达水平、克隆形成数、迁移细胞数降低（P均<0.001），抑制率、凋亡率升高（P均<0.001）。miR-383-5p分别与PCED1B-AS1、PRDX3特异性结合。抑制miR-383-5p表达可减弱下调PCED1B-AS1对LoVo细胞增殖、迁移、克隆形成、凋亡的影响（P均<0.001）。［结论］ 下调PCED1B-AS1通过靶向上调miR-383-5p表达可抑制CRC细胞增殖和迁移，诱导细胞凋亡，进而抑制CRC进展。 |
| 英文摘要: |
| Abstract：［Objective］ To investigate the role of long non-coding RNA(lncRNA) PCED1B-AS1/miR-383-5p axis on the progression of colorectal cancer(CRC). ［Methods］ Surgical samples of tumor tissues and adjacent tissues were collected from 41 CRC patients who were treated in South Campus of the Fifth Medical Center， PLA General Hospital from January 2018 to October 2019. The expression levels of PCED1B-AS1， miR-383-5p and peroxidase 3(PRDX3) mRNA were detected by RT-qPCR. CRC LoVo cells were transfected with si-NC， si-PCED1B-AS1， miR-NC， miR-383-5p mimics， si-PCED1B-AS1+anti-miR-NC and si-PCED1B-AS1+anti-miR-383-5p， respectively. And cell proliferation， colony formation ability， migration and apoptosis were detected with CCK-8 method， colony formation assay， Transwell assay and flow cytometry， respectively. Dual luciferase reporter assay was used to confirm the targeting relationship between miR-383-5p and PCED1B-AS1 or PRDX3. ［Results］ Compared with adjacent tissues， the expression of PCED1B-AS1（0.92±0.12 vs 2.87±0.32， P<0.05） and PRDX3 mRNA(0.93±0.11 vs 2.30±0.26， P<0.05） in CRC tissue was significantly increased， and the expression level of miR-383-5p was decreased(0.98±0.15 vs 0.40±0.05， P<0.001). After down-regulating PCED1B-AS1， the expression level of miR-383-5p(1.00±0.00 vs 2.95±0.12， P<0.001)， inhibition rate(0 vs 47.75%±2.75%， P<0.05)， and apoptosis rate(8.10%±0.75% vs 20.20%±1.09%， P<0.001) of LoVo cells were signifivantly increased； PRDX3 mRNA expression level(1.00±0.00 vs 0.27±0.03， P<0.001)， the numbers of colonies(116.78±6.01 vs 67.56±4.11， P<0.001) and migrated cells(173.78±8.32 vs 85.89±3.07， P<0.001) were significantly decreased. After the overexpression of miR-383-5p， PRDX3 mRNA expression level in LoVo cells， the numbers of colonies and migrated LoVo cells were decreased(all P<0.001)， and the inhibition rate and apoptosis rate of LoVo cells were increased(all P<0.001). miR-383-5p was specifically bound to PCED1B-AS1 and PRDX3， respectively. miR-383-5p inhibition could attenuate the effect of PCED1B-AS1 down-regulation on the proliferation， migration， and apoptosis of LoVo cells(all P<0.001). ［Conclusion］ Down-regulation of PCED1B-AS1 inhibits CRC cell proliferation， migration， and induces cell apoptosis by up-regulating miR-383-5p in a targeted manner， thereby inhibiting the progression of CRC. |
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