Long noncoding RNA plasmacytoma variant translocation 1 promotes progression of colorectal cancer by sponging microRNA-152-3p and regulating E2F3/MAPK8 signaling.
Long noncoding RNA plasmacytoma variant translocation 1 promotes progression of colorectal cancer by sponging microRNA-152-3p and regulating E2F3/MAPK8 signaling.
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DOI：
10.1111/cas.15113
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发表时间：
2022-01
期刊：
影响因子：
5.7
通讯作者：
Liu J
中科院分区：
文献类型：
--
作者：
Liu X;Li L;Bai J;Li L;Fan J;Fu Z;Liu J
本研究的目的是探讨结直肠癌（CRC）的发病机制和长非编码RNA浆细胞瘤变异易位1（PVT 1）在CRC进展中的作用。生物信息学分析验证了PVT 1在肿瘤和正常组织中的表达。定量PCR和蛋白质印迹分别用于测量mRNA和蛋白质水平。采用MTT法、Transwell法、集落形成法和体内实验检测PVT 1对结直肠癌细胞增殖、迁移和侵袭的影响。使用FISH测定显示PVT 1和microRNA（miR）-152 - 3 p在CRC细胞中共定位。通过生物信息学分析、荧光素酶分析和RNA pull-down分析对miR-152 - 3 p的靶基因进行预测和验证。ChIP分析显示E2 F3与MAPK 8的启动子结合。我们发现PVT 1在结直肠癌标本中过表达，并且其在结直肠癌细胞中的表达高于正常肠细胞。PVT 1的过表达增强了CRC细胞的增殖、迁移和侵袭，而PVT 1的敲低抑制了这些过程。MicroRNA-152 - 3 p是PVT 1的靶标，E2 F3是miR-152 - 3 p的靶标。挽救实验证实了miR-152 - 3 p与PVT 1之间以及miR-152 - 3 p与E2 F3之间的相互作用。荧光素酶和ChIP测定结果证实，E2 F3调节MAPK 8的转录激活。长非编码RNA PVT 1通过海绵化miR-152 - 3 p激活E2 F3信号传导。PVT 1/miR-152 - 3 p/E2 F3/MAPK 8轴促进CRC进展。浆细胞瘤变体易位1（PVT 1）通过海绵状microRNA（miR）-152-3p激活E2 F3信号传导。PVT 1/miR-152 - 3 p/E2 F3/MAPK 8轴促进结直肠癌进展。
The purpose of this study was to investigate the pathogenesis of colorectal cancer (CRC) and the effects of the long noncoding RNA plasmacytoma variant translocation 1 (PVT1) on CRC progression. Bioinformatics analysis verified PVT1 expression in tumor and normal tissues. Quantitative PCR and western blotting were used to measure mRNA and protein levels, respectively. The MTT, Transwell, colony formation, and in vivo assays were used to assess the effects of PVT1 on proliferation, migration, and invasion by CRC cells. Both PVT1 and microRNA (miR)‐152‐3p were shown to be colocalized in CRC cells using FISH assay. The target genes of miR‐152‐3p were predicted and verified by bioinformatics analysis, luciferase assay, and RNA pull‐down assay. The ChIP assay revealed that E2F3 binds with the promoter of MAPK8. We found that PVT1 was overexpressed in CRC specimens, and its expression was higher in CRC cells than normal intestinal cells. Overexpression of PVT1 enhanced the proliferation, migration, and invasion of CRC cells, whereas PVT1 knockdown inhibited these processes. MicroRNA‐152‐3p was a target of PVT1, and E2F3 was a target of miR‐152‐3p. Rescue experiments confirmed the interaction between miR‐152‐3p and PVT1 and between miR‐152‐3p and E2F3. Luciferase and ChIP assay results confirmed that E2F3 modulates the transcriptional activation of MAPK8. Long noncoding RNA PVT1 activated E2F3 signaling by sponging miR‐152‐3p. The PVT1/miR‐152‐3p/E2F3/MAPK8 axis promoted CRC progression. Plasmacytoma variant translocation 1 (PVT1) activated E2F3 signaling by sponging microRNA (miR)‐152‐3p. The PVT1/miR‐152‐3p/E2F3/MAPK8 axis promoted colorectal cancer progression.
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影响因子：
8.8
作者：
Takahashi, Y.;Sawada, G.;Kurashige, J.;Uchi, R.;Matsumura, T.;Ueo, H.;Takano, Y.;Eguchi, H.;Sudo, T.;Sugimachi, K.;Yamamoto, H.;Doki, Y.;Mori, M.;Mimori, K.
通讯作者：
Mimori, K.
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影响因子：
8
作者：
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通讯作者：
Liu, Yanrong
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影响因子：
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作者：
Zhong W;Chen S;Zhang Q;Xiao T;Qin Y;Gu J;Sun B;Liu Y;Jing X;Hu X;Zhang P;Zhou H;Sun T;Yang C
通讯作者：
Yang C
影响因子：
3.1
作者：
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影响因子：
4.6
作者：
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通讯作者：
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