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An endogenous and ectopic expression of metabotropic glutamate receptor 8 (mGluR8) inhibits proliferation and increases chemosensitivity of human neuroblastoma and glioma cells.代谢型谷氨酸受体 8（mGluR8）的内源性和异位表达抑制人神经母细胞瘤和神经胶质瘤细胞的增殖并增加其化学敏感性。
Cancer Lett. 2018 Sep 28;432:1-16. doi: 10.1016/j.canlet.2018.06.004. Epub 2018 Jun 6.
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miR-570 Inhibits Proliferation, Angiogenesis, and Immune Escape of Hepatocellular Carcinoma.miR-570 抑制肝癌的增殖、血管生成和免疫逃逸。
Cancer Biother Radiopharm. 2018 Aug;33(6):252-257. doi: 10.1089/cbr.2017.2389. Epub 2018 Jun 6.
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transgenic zebrafish models identify as a mediator of rhabdomyosarcoma tumorigenesis.转基因斑马鱼模型将 鉴定为横纹肌肉瘤发生的介质。
Elife. 2018 Jun 5;7:e33800. doi: 10.7554/eLife.33800.
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MiR-23a regulates the proliferation and migration of human pulmonary artery smooth muscle cells (HPASMCs) through targeting BMPR2/Smad1 signaling.miR-23a 通过靶向 BMPR2/Smad1 信号通路调节人肺动脉平滑肌细胞（HPASMCs）的增殖和迁移。
Biomed Pharmacother. 2018 Jul;103:1279-1286. doi: 10.1016/j.biopha.2018.04.172. Epub 2018 May 7.
5
MiR-519d inhibits prostate cancer cell proliferation, cycle and invasion via targeting NRBP1.miR-519d 通过靶向 NRBP1 抑制前列腺癌细胞增殖、周期和侵袭。
Eur Rev Med Pharmacol Sci. 2018 May;22(10):2985-2990. doi: 10.26355/eurrev_201805_15054.
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Control of PD-L1 expression by miR-140/142/340/383 and oncogenic activation of the OCT4-miR-18a pathway in cervical cancer.宫颈癌中 miR-140/142/340/383 对 PD-L1 表达的调控和 OCT4-miR-18a 通路的致癌激活。
Oncogene. 2018 Sep;37(39):5257-5268. doi: 10.1038/s41388-018-0347-4. Epub 2018 May 31.
7
Stemness-Attenuating miR-503-3p as a Paracrine Factor to Regulate Growth of Cancer Stem Cells.作为旁分泌因子的干性衰减型miR-503-3p调控癌症干细胞的生长
Stem Cells Int. 2018 Apr 4;2018:4851949. doi: 10.1155/2018/4851949. eCollection 2018.
8
LncRNA MALAT1/miR-129 axis promotes glioma tumorigenesis by targeting SOX2.长链非编码RNA MALAT1/微小RNA-129轴通过靶向SOX2促进胶质瘤的肿瘤发生。
J Cell Mol Med. 2018 Aug;22(8):3929-3940. doi: 10.1111/jcmm.13667. Epub 2018 May 29.
9
RETRACTED: NY-SAR-35 is involved in apoptosis, cell migration, invasion and epithelial to mesenchymal transition in glioma.撤回：NY-SAR-35 参与了神经胶质瘤中的细胞凋亡、细胞迁移、侵袭和上皮间质转化。
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10
Immunosuppressive effects of hypoxia-induced glioma exosomes through myeloid-derived suppressor cells via the miR-10a/Rora and miR-21/Pten Pathways.缺氧诱导的脑胶质瘤外泌体通过髓源抑制性细胞通过 miR-10a/Rora 和 miR-21/Pten 通路发挥免疫抑制作用。
Oncogene. 2018 Aug;37(31):4239-4259. doi: 10.1038/s41388-018-0261-9. Epub 2018 May 1.

微小RNA-485-5p通过直接靶向配对盒3来减弱胶质瘤中的细胞增殖。

MicroRNA-485-5p attenuates cell proliferation in glioma by directly targeting paired box 3.

作者信息

Wang Ren, Zuo Xiaohua, Wang Kai, Han Qiu, Zuo Jiandong, Ni Hongzao, Liu Wenguang, Bao Hongguang, Tu Yiming, Xie Peng

机构信息

Department of Pediatric Surgery, Huai'an Women and Children's Hospital Huai'an 223002, Jiangsu, PR China.

Department of Pain Management, Huai'an Hospital Affiliated to Xuzhou Medical University, Second People's Hospital of Huai'an Huai'an, Jiangsu, PR China.

出版信息

Am J Cancer Res. 2018 Dec 1;8(12):2507-2517. eCollection 2018.

PMID:30662807
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6325470/
Abstract

MicroRNA-485-5p (miR-485-5p) has been reported to be involved in the development and progression of human cancers; however, its role in glioma remains unclear. In the present study, we found that miR-485-5p was significantly down-regulated in both glioma tissues and cell lines. Functional experiments indicated that enhanced expression of miR-485-5p attenuated glioma cell proliferation in vitro and in vivo, and induced glioma cells cycle arrest in G1. MiR-485-5p was found to directly bind to the 3'-UTR of paired box 3 (PAX3) and decrease its expression of protein level, which further inhibits the proliferation of glioma. The decreasing of PAX3 was found to lead to the accumulation of p-JNK. Mechanistic studies revealed that restoring the expression of PAX3 alleviated miR-485-5p-induced inhibition of proliferation of glioma cells. Taken together, these findings suggest that PAX3 modulation by miR-485-5p has an important role in regulating glioma proliferation, and miR-485-5p might be a novel therapeutic target for glioma.

摘要

据报道，微小RNA-485-5p（miR-485-5p）参与人类癌症的发生和发展；然而，其在胶质瘤中的作用仍不清楚。在本研究中，我们发现miR-485-5p在胶质瘤组织和细胞系中均显著下调。功能实验表明，miR-485-5p表达增强可在体外和体内减弱胶质瘤细胞增殖，并诱导胶质瘤细胞在G1期发生细胞周期阻滞。发现miR-485-5p直接结合配对盒3（PAX3）的3'-非翻译区并降低其蛋白水平表达，进而抑制胶质瘤增殖。发现PAX3减少会导致p-JNK积累。机制研究表明，恢复PAX3表达可减轻miR-485-5p诱导的胶质瘤细胞增殖抑制。综上所述，这些发现表明miR-485-5p对PAX3的调控在调节胶质瘤增殖中起重要作用，miR-485-5p可能是胶质瘤的一个新的治疗靶点。