LINC00467 Promotes Prostate Cancer Progression via M2 Macrophage Polarization and the miR-494-3p/STAT3 Axis.
LINC00467 Promotes Prostate Cancer Progression via M2 Macrophage Polarization and the miR-494-3p/STAT3 Axis.
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LINC00467 通过 M2 巨噬细胞极化和 miR-494-3p/STAT3 轴促进前列腺癌进展
DOI：
10.3389/fonc.2021.661431
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发表时间：
2021
影响因子：
4.7
通讯作者：
Wang G
中科院分区：
文献类型：
--
作者：
Jiang H;Deng W;Zhu K;Zeng Z;Hu B;Zhou Z;Xie A;Zhang C;Fu B;Zhou X;Wang G
研究背景长链非编码RNA LINC 00467在许多恶性肿瘤中起着重要作用。然而，LINC 00467在前列腺癌（PC）中的作用尚不清楚。在此，我们旨在探索LINC 00467调节PC进展的机制。方法采用生物信息学分析和RT-qPCR方法，检测LINC 00467在PC组织和细胞中的表达。通过功能丧失实验证实LINC 00467在PC进展中的功能。通过CCK-8和EdU测定来评估PC细胞增殖。流式细胞仪检测PC细胞的细胞周期进程。此外，用Transwell法研究PC细胞的迁移和侵袭。Western blot检测上皮-间质转化相关因子的表达。通过RT-qPCR证实LINC 00467与前列腺癌进展和M2巨噬细胞极化的相互作用。LINC 00467的亚细胞定位是通过细胞核和细胞质RNA的分级分离来研究的。生物信息学数据分析用于预测LINC 00467表达与miR-494- 3 p表达的相关性。通过使用双荧光素酶报告系统鉴定LINC 00467/miR-494- 3 p/STAT 3相互作用。最后，LINC 00467表达对PC进展的影响用体内肿瘤发生的裸鼠模型研究。结果LINC 00467在PC组织和细胞中表达上调。下调LINC 00467表达抑制PC细胞生长、细胞周期进展、迁移和侵袭。下调的LINC 00467表达通过M2巨噬细胞极化类似地抑制PC细胞迁移。Western blot分析表明LINC 00467对STAT 3信号通路有调节作用。我们确定LINC 00467主要定位于细胞质。生物信息学分析和拯救实验表明，LINC 00467通过miR-494- 3 p/STAT 3轴促进PC进展。下调的LINC 00467表达也能够抑制体内PC肿瘤生长。结论LINC 00467通过M2巨噬细胞极化和miR-494- 3 p/STAT 3轴促进前列腺癌进展。
Background The long non-coding RNA LINC00467 plays a vital role in many malignancies. Nevertheless, the role of LINC00467 in prostate carcinoma (PC) is unknown. Herein, we aimed to explore the mechanism by which LINC00467 regulates PC progression. Methods We used bioinformatics analyses and RT-qPCR to investigate the expression of LINC00467 in PC tissues and cells. The function of LINC00467 in the progression of PC was confirmed by loss-of-function experiments. PC cell proliferation was assessed by CCK-8 and EdU assays. The cell cycle progression of PC cells was examined by flow cytometry. Moreover, Transwell assays were used to investigate the migration and invasion of PC cells. Western blot assays were used to detect the expression of factors associated with epithelial–mesenchymal transition. The interactions of LINC00467 with prostate cancer progression and M2 macrophage polarization were confirmed by RT-qPCR. The subcellular localization of LINC00467 was investigated via the fractionation of nuclear and cytoplasmic RNA. Bioinformatics data analysis was used to predict the correlation of LINC00467 expression with miR-494-3p expression. LINC00467/miR-494-3p/STAT3 interactions were identified by using a dual-luciferase reporter system. Finally, the influence of LINC00467 expression on PC progression was investigated with an in vivo nude mouse model of tumorigenesis. Results We established that LINC00467 expression was upregulated in PC tissues and cells. Downregulated LINC00467 expression inhibited PC cell growth, cell cycle progression, migration, and invasion. Downregulated LINC00467 expression similarly inhibited PC cell migration via M2 macrophage polarization. Western blot analysis showed that LINC00467 could regulate the STAT3 pathway. We established that LINC00467 is mainly localized to the cytoplasm. Bioinformatics analysis and rescue experiments indicated that LINC00467 promotes PC progression via the miR-494-3p/STAT3 axis. Downregulated LINC00467 expression was also able to suppress PC tumor growth in vivo. Conclusions Our study reveals that LINC00467 promotes prostate cancer progression via M2 macrophage polarization and the miR-494-3p/STAT3 axis.
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影响因子：
8
作者：
Petrovics, G;Zhang, W;Srivastava, S
通讯作者：
Srivastava, S
影响因子：
254.7
作者：
Jemal, Ahmedin;Siegel, Rebecca;Thun, Michael J.
通讯作者：
Thun, Michael J.
影响因子：
10.5
作者：
Cabili, Moran N.;Trapnell, Cole;Rinn, John L.
通讯作者：
Rinn, John L.
DOI：
10.4149/bll_2018_095
发表时间：
2018-01-01
影响因子：
1.5
作者：
Mazalova, L.;Sladek, Z.;Masarik, M.
通讯作者：
Masarik, M.
CERNA假设：隐藏RNA语言的Rosetta石头？
影响因子：
64.5
作者：
Salmena L;Poliseno L;Tay Y;Kats L;Pandolfi PP
通讯作者：
Pandolfi PP