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lncRNA HLA Complex Group 18 (HCG18) Facilitated Cell Proliferation, Invasion, and Migration of Prostate Cancer Through Modulating miR-370-3p/DDX3X Axis
Long non-coding RNAs (lncRNAs) have been reported to exert critical functions in the malignant development of many cancers. lncRNA HLA complex group 18 (HCG18) has been confirmed to have a promoting effect on various cancers. However, whether HCG18 functions in PC is still unclear. Therefore, the cu...
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Published in: | Reproductive sciences (Thousand Oaks, Calif.) Calif.), 2021-12, Vol.28 (12), p.3406-3416 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Long non-coding RNAs (lncRNAs) have been reported to exert critical functions in the malignant development of many cancers. lncRNA HLA complex group 18 (HCG18) has been confirmed to have a promoting effect on various cancers. However, whether HCG18 functions in PC is still unclear. Therefore, the current study aimed at unveiling the role of HCG18 in PC progression and its regulatory mechanism on the biological behaviors of PC. Here, RT-qPCR was utilized to detect HCG18 expression, and then, functional experiments were conducted to verify the effects of HCG18 on PC cell proliferation, migration, invasion, and apoptosis. According to the results, HCG18 was significantly up-regulated in PC cells and it facilitated cell proliferation, migration, and invasion in PC. Furthermore, a series of mechanism experiments were carried out to verify the relationship among HCG18, miR-370-3p, and DEAD-box helicase 3 X-linked(DDX3X) in PC cells. Final rescue assays showed that DDX3X overexpression could reverse the inhibitory function of silencing HCG18 on PC progression. In summary, our study showed that lncRNA HCG18 accelerated cell proliferation, invasion, and migration of PC via up-regulating DDX3X through sponging miR-370-3p, providing a novel finding about PC-related regulatory mechanism. |
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ISSN: | 1933-7191 1933-7205 |
DOI: | 10.1007/s43032-021-00614-2 |