miR-217 suppresses proliferation and promotes apoptosis in cardiac myxoma by targeting Interleukin-6
- Department of Oncology, Huaihe Hospital of Henan University, Kaifeng, 475000 (China)
- Department of Cardiovascular Medicine, Huaihe Hospital of Henan University, Kaifeng, 475000 (China)
- Department of Geriatric Cardiovascular Medicine, Huaihe Hospital of Henan University, Kaifeng, 475000 (China)
Cardiac myxoma (CM) is a prevalent primary cardiac tumor. miR-217 plays a vital role in tumorigenesis of various cancers, however, its role and underlying molecular mechanism in human CM remain poorly understood. Here, we reported that the expression of miR-217 was downregulated in CM tissues and inversely correlated with the expression of Interleukin-6 (IL-6) mRNA. Gain-of-function analysis indicated that overexpression of miR-217 inhibited the proliferation and promoted the apoptosis of the primary CM cells. Bioinformatics analysis showed that IL-6 was a direct target gene of miR-217, which is confirmed by the dual luciferase assays. Moreover, downregulation of IL-6 by small interference RNA (siRNA) mimicked the tumor-suppressive effects of miR-217 in CM. Furthermore, rescue experiments pointed out that restoration of IL-6 expression abrogated the anti-proliferative and pro-apoptotic effect induced by miR-217 overexpression in CM cells. Taken together, we validated that miR-217 could act as a tumor suppressor in CM by directly targeting 3′UTR of IL-6 gene, indicating that manipulation of miR-217 may be a potential therapeutic strategy for CM patients. - Highlights: • Lower expression of miR-217 and higher expression of IL-6 mRNA was observed in CM tissues. • miR-217 overexpression suppressed proliferation and promoted apoptosis of primary CM cells. • miR-217 targeted IL-6 3′-UTR to inhibit its expression. • Reintroduction of IL-6 reversed the effect of miR-217 overexpression on CM cell proliferation and apoptosis.
- OSTI ID:
- 22719047
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 490, Issue 3; Other Information: Copyright (c) 2017 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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