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长链非编码RNA MORT通过上调miRNA-16抑制套细胞淋巴瘤中的癌细胞增殖并促进细胞凋亡。

LncRNA MORT Inhibits Cancer Cell Proliferation and Promotes Apoptosis in Mantle Cell Lymphoma by Upregulating miRNA-16.

作者信息

Tang Xiaoqiong, Long Yaoying, Xu Liuyue, Yan Xinyu

机构信息

Department of Hematology, The First Affiliated Hospital of Chongqing Medical University, Chongqing City 400016, People's Republic of China.

出版信息

Cancer Manag Res. 2020 Mar 23;12:2119-2125. doi: 10.2147/CMAR.S233859. eCollection 2020.

DOI:10.2147/CMAR.S233859
PMID:32280273
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7127878/
Abstract

INTRODUCTION

LncRNA mortal obligate RNA transcript (MORT) is downregulated in different types of cancer, indicating its involvement in cancer biology.

METHODS

In this study, MORT and miRNA-16 were both downregulated in plasma of mantle cell lymphoma (MCL) patients than that in the controls. The low levels of MORT and miRNA-16 were correlated with poor survival of MCL patients. The expression of MORT and miRNA-16 was positively correlated only in MCL patients.

RESULTS

Overexpression of MORT and miRNA-16 suppressed cell proliferation but promoted cancer cell apoptosis, while miRNA-16 inhibitor reduced the effects of MORT overexpression. Overexpression of MORT led to upregulated expression of miRNA-16, while overexpression of miRNA-16 had no effect on the expression of MORT.

CONCLUSION

Therefore, MORT may inhibit cancer cell proliferation and promote apoptosis in mantle cell lymphoma by upregulating miRNA-16.

摘要

引言

长链非编码RNA必死性专性RNA转录本（MORT）在不同类型癌症中表达下调，表明其参与癌症生物学过程。

方法

在本研究中，套细胞淋巴瘤（MCL）患者血浆中MORT和miRNA-16的表达均低于对照组。MORT和miRNA-16水平低与MCL患者生存率低相关。MORT和miRNA-16的表达仅在MCL患者中呈正相关。

结果

MORT和miRNA-16过表达抑制细胞增殖，但促进癌细胞凋亡，而miRNA-16抑制剂可降低MORT过表达的作用。MORT过表达导致miRNA-16表达上调，而miRNA-16过表达对MORT的表达无影响。

结论

因此，MORT可能通过上调miRNA-16抑制套细胞淋巴瘤癌细胞增殖并促进其凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5125/7127878/b47e420aeeab/CMAR-12-2119-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5125/7127878/102cdd5829ab/CMAR-12-2119-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5125/7127878/a4927a1c3cc1/CMAR-12-2119-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5125/7127878/d0355293c39a/CMAR-12-2119-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5125/7127878/75563ab997cd/CMAR-12-2119-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5125/7127878/fdb87bf061df/CMAR-12-2119-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5125/7127878/b47e420aeeab/CMAR-12-2119-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5125/7127878/102cdd5829ab/CMAR-12-2119-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5125/7127878/a4927a1c3cc1/CMAR-12-2119-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5125/7127878/d0355293c39a/CMAR-12-2119-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5125/7127878/75563ab997cd/CMAR-12-2119-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5125/7127878/fdb87bf061df/CMAR-12-2119-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5125/7127878/b47e420aeeab/CMAR-12-2119-g0006.jpg

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