Home Neoplasma 2018 Neoplasma Vol.65, No.3, p.331-338, 2018

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Founded: 1954
ISSN 0028-2685
ISSN 1338-4317 (online)

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Neoplasma Vol.65, No.3, p.331-338, 2018

Title: miR-506 suppresses cervical cancer cell proliferation both in vitro and in vivo
Author: M. GONG, C. CHEN, H. ZHAO, M. SUN, M. SONG

Abstract: Cervical cancer (CC) is one of the most common gynecological malignancies in women worldwide. Recently, increasing evidence indicates aberrant expression of miR-506, which was reported to be associated with a variety of tumors. The aim of this study was to evaluate the potential role of miR-506 in CC and to verify its effect on the regulation of ABCC4. The expression of miR-506 in cervical cancer tissues, HeLa and C33A cell lines was examined using quantitative Real-time PCR. MTT assay and animals studies were used to examine the effects of miR-506 on cervical cancer proliferation. Luciferase reporter and western blot were used to confirm that miR-506 could regulate ABCC4. We found that miR-506 was signifi- cantly downregulated in human CC cell lines (HeLa and C33A) and clinical CC specimens as compared to matched cell lines and adjacent normal tissues, while the expression level of ABCC4 was higher in tumor tissues than in the adjacent normal tissues. We also revealed that up-regulated expression of miR-506 could inhibit CC cells proliferation both in vitro and in vivo. Moreover, ABCC4 was identified as a direct target of miR-506 and the inverse relationship between them was also observed. In summary, our findings suggest that miR-506 has an important role in suppressing CC cell proliferation and suppresses the expression of ABCC4 by directly targeting its 3’-UTR. miR-506 may represent a novel therapeutic target of microRNA-mediated suppression of cell proliferation in CC, but the role of the miR-506/ABCC4 axis in CC progression needs further study.

Keywords: miR-506, ABCC4, cervical cancer, proliferation
Published online: 16-May-2018
Year: 2018, Volume: 65, Issue: 3 Page From: 331, Page To: 338
doi:10.4149/neo_2018_170112N25


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