MicroRNA-525 enhances chondrosarcoma malignancy by targeting F-spondin 1.

Abstract:

:Increasing evidence has suggested that microRNAs (miRNAs; miRs) are extensively involved in the progression of chondrosarcoma (CHS). However, few studies have investigated the functional role of miR-525 in CHS tissues and cells. In the present study, it was discovered that miR-525 levels were decreased in CHS tissues and cells. Dual luciferase assays indicated that F-spondin 1 (SPON1) is a target gene of microRNA (miR)-525. In addition, miR-525 overexpression suppressed SW1353 cell migration and invasion and enhanced SW1353 cell apoptosis. Increased SPON1 expression levels were identified in CHS tissues and cell lines. Furthermore, miR-525 overexpression significantly suppressed the activation of focal adhesion kinase (FAK)/Src/phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/protein kinase B (Akt) signaling in CHS cells; this suppression led to SPON1 silencing. In comparison, the SPON1 knockdown-mediated inactivation of FAK/Src/PI3K/Akt signaling was inhibited by inhibiting miR-525. In summary, the present study revealed that decreased miR-525 levels could enhance CHS malignancy as decreased miR-525 binding to the 3' untranslated region of SPON1 activates FAK/Src/PI3K/Akt signaling.

journal_name

Oncol Lett

journal_title

Oncology letters

authors

Liu B,Song X,Yan Z,Yang H,Shi Y,Wu J

doi

10.3892/ol.2018.9711

subject

Has Abstract

pub_date

2019-01-01 00:00:00

pages

781-788

issue

1

eissn

1792-1074

issn

1792-1082

pii

OL-0-0-9711

journal_volume

17

pub_type

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