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微小RNA-302a通过靶向Rad52使白血病细胞对依托泊苷敏感。

MiR-302a sensitizes leukemia cells to etoposide by targeting Rad52.

作者信息

Liu Xiaoning, Heng Chun, Li Yuanyuan, Yu Liang

机构信息

Central Laboratory, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu Province, 223300, China.

Hematology Department, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu Province, 223300, China.

出版信息

Oncotarget. 2017 May 16;8(43):73884-73891. doi: 10.18632/oncotarget.17878. eCollection 2017 Sep 26.

DOI:10.18632/oncotarget.17878
PMID:29088754
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5650309/
Abstract

miR-302a have been reported to participate in various physiological and pathological processes, however, a role for miR-302a in etoposide (VP-16) resistance of acute myeloid leukemia (AML) has not been reported. In this study, the aberrant expression of miR-302a was analyzed in patients with AML and in the AML HL-60 and U937 cell lines. Overexpression of miR-302a, by targeting the 3'UTR of Rad52, enhanced VP-16 sensitivity in the HL-60 and U937 cell. Accordingly, knockdown of Rad52 sensitized the HL-60 and U937 cells to VP-16-induced apoptosis and proliferation suppression. In addition, miR-302a enhanced the tumor-suppressive effect of VP-16 in a xenograft model of human HL-60 and U937 cell lines. Moreover, miR-302a repressed the AKT/Gsk3β/β-catenin pathway after Rad52 inhibition. Reintroduction of Rad52 reversed miR-302a-induced signaling suppression. The results of the present study demonstrated that miR-302a may be a target for the treatment of AML and a potential indicator of the therapeutic sensitivity of AML to VP-16.

摘要

据报道，miR-302a参与多种生理和病理过程，然而，miR-302a在急性髓系白血病（AML）对依托泊苷（VP-16）耐药中的作用尚未见报道。在本研究中，分析了AML患者以及AML HL-60和U937细胞系中miR-302a的异常表达。通过靶向Rad52的3'UTR过表达miR-302a可增强HL-60和U937细胞对VP-16的敏感性。相应地，敲低Rad52可使HL-60和U937细胞对VP-16诱导的凋亡和增殖抑制敏感。此外，在人HL-60和U937细胞系的异种移植模型中，miR-302a增强了VP-16的肿瘤抑制作用。此外，miR-302a在抑制Rad52后抑制AKT/Gsk3β/β-连环蛋白通路。重新引入Rad52可逆转miR-302a诱导的信号抑制。本研究结果表明，miR-302a可能是治疗AML的靶点，也是AML对VP-16治疗敏感性的潜在指标。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c1/5650309/2e851f8ee473/oncotarget-08-73884-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c1/5650309/54f09a84c122/oncotarget-08-73884-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c1/5650309/ca0c7c346b1a/oncotarget-08-73884-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c1/5650309/b2c571585d9a/oncotarget-08-73884-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c1/5650309/79800d66b601/oncotarget-08-73884-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c1/5650309/11c045f8dbfe/oncotarget-08-73884-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c1/5650309/2e851f8ee473/oncotarget-08-73884-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c1/5650309/54f09a84c122/oncotarget-08-73884-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c1/5650309/ca0c7c346b1a/oncotarget-08-73884-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c1/5650309/b2c571585d9a/oncotarget-08-73884-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c1/5650309/79800d66b601/oncotarget-08-73884-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c1/5650309/11c045f8dbfe/oncotarget-08-73884-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c1/5650309/2e851f8ee473/oncotarget-08-73884-g006.jpg

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