RESUMEN
OBJECTIVE: To clarify the role of IGF-2 on the development of myopia, the dynamic expression of IGF-2 was investigated in the FD eyes' retina, and the effects of intravitreous injection with IGF-2 ASON was studied on the diopter and axial eye length of FD eyes. METHODS: 64 guinea pigs were divided into 2 groups. In group A (n = 24), the right eyes were covered. On days 7, 14 and 21, the diopter, axial eye length and level of IGF-2 of both eyes were measured in every 8 guinea pigs. In group B (n = 40), the right eyes were covered. On day 1, the right eyes were received intravitreal injection with 40 µg IGF-2SON, 10 µg, 20 µg or 40 µg IGF-2 ASON. The diopter, axial eye length and level of IGF-2 were measured on day 14. RESULTS: FD eyes showed myopic shift, axial length enlongation, and up-regulation in retinal IGF-2 from day 7 to day 21. The level of retinal IGF-2 in FD eyes was higher than that in non-FD eyes. Compare with FD eyes without injection, the myopia diopter of FD eyes decreased in received intravitreous injection with IGF-2 ASON, axial length shortened, and down-regulated with retinal IGF-2. With the increase dose of IGF-2 ASON, the change of myopic diopter, axial length, and level of retinal IGF-2 were showed more and more significant. CONCLUSIONS: FD is effective to up-regulate the level of retinal IGF-2 expression in guinea pig. Intravitreous injection with IGF-2 ASON can inhibit the development of myopia.
Asunto(s)
Modelos Animales de Enfermedad , Regulación de la Expresión Génica/efectos de los fármacos , Factor II del Crecimiento Similar a la Insulina/genética , Miopía/prevención & control , Oligonucleótidos Antisentido/administración & dosificación , Retina/metabolismo , Animales , Longitud Axial del Ojo , Western Blotting , Cobayas , Inyecciones Intravítreas , Liposomas , Miopía/metabolismo , ARN Mensajero/metabolismo , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Regulación hacia ArribaRESUMEN
Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the data shown for the cell invasion assays in Figs. 2C and 4C were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 18: 595602, 2018; DOI: 10.3892/mmr.2018.8979].
RESUMEN
A number of studies have highlighted that aberrantly expressed microRNAs (miRNAs/miRs) serve crucial roles in the tumorigenesis and tumor development of retinoblastoma (RB). Hence, a full investigation of the biological roles and regulatory mechanisms of miRNAs in RB may provide novel therapeutic targets for patients with this malignancy. miR198 is frequently abnormally expressed in various types of human cancers. However, the expression level, biological roles and underlying mechanisms of miR198 in RB remain to be elucidated. In the present study, miR198 expression was upregulated in RB tissues and cell lines. Silencing of miR198 attenuated cell proliferation and invasion in RB. In addition, phosphatase and tensin homolog deleted on chromosome ten (PTEN) was predicted as a potential target of miR198 using bioinformatics analysis. Subsequent luciferase reporter assay indicated that the 3'untranslated region of PTEN can be directly targeted by miR198. Furthermore, miR198 inhibition increased the PTEN expression at the mRNA and protein levels in RB cells. In addition, PTEN mRNA expression was downregulated in RB tissues, and this downregulation was inversely associated with the expression level of miR198. PTEN knockdown rescued the inhibitory effects of miR198 underexpression on cell proliferation and invasion in RB. Notably, the downregulation of miR198 inactivated the phosphoinositide 3kinase (PI3K)/protein kinase B (AKT) signaling pathway in RB. These results demonstrated that miR198 may serve oncogenic roles in RB by directly targeting PTEN and regulating the PI3K/AKT signaling pathway. Hence, miR198 may be a promising therapeutic target for patients with RB.