<p>microRNA-605 directly targets SOX9 to alleviate the aggressive phenotypes of glioblastoma multiforme cell lines by deactivating the PI3K/Akt pathway</p>

Abstract

Background Aberrant microRNA (miRNA) expression has been widely reported to play a crucial role in the progression and development of glioblastoma (GBM). miR-605 has been identified as a tumor-suppressing miRNA in several types of human cancers. Nevertheless, the expression profile and detailed roles of miR-605 in GBM remain unclear and need to be further elucidated. Materials and methods RT-qPCR analysis was utilized for the determination of miR-605 expression in GBM tissues and cell lines. In addition, CCK-8 assay, transwell migration and invasion assays, as well as sub-cutaneous xenograft mouse models were utilized to evaluate the effects of miR-605 upregulation in GBM cells. Notably, the potential mechanisms underlying the activity of miR-605 in the malignant phenotypes of GBM were explored. Results We observed that expression of miR-605 was reduced in GBM tissues and cell lines. Decreased miR-605 expression exhibited significant correlation with KPS score. The overall survival rate in GBM patients with low miR-605 expression was lower than that of patients with high miR-605 expression. Increased miR-605 expression suppressed the proliferation, migration, and invasion of U251 and T98 cells. In addition, miR-605 upregulation impaired tumor growth in vivo. Furthermore, SRY-Box 9 (SOX9) was identified as a direct target gene of miR-605 in U251 and T98 cells. SOX9 expression was shown to exhibit an inverse correlation with miR-605 expression in GBM tissues. Moreover, silencing of SOX9 expression mimicked the tumor-suppressing roles of miR-605 in U251 and T98 cells, while SOX9 restoration rescued the suppressive effects of miR-605 overexpression in the same. Notably, miR-605 suppressed the PI3K/Akt pathway in GBM in vitro and in vivo. Conclusion These results demonstrated that miR-605 acts as a tumor suppressor in the development of GBM by directly targeting SOX9 and inhibiting the activation of the PI3K/Akt pathway, suggesting its potential role as a therapeutic target for GBM.

Long noncoding RNA SNHG14 promotes�the�aggressiveness of retinoblastoma by sponging microRNA‑124 and thereby upregulating STAT3

“…Mouse xenograft tumor model. All experimental procedures involving animals were conducted in accordance with the Animal Protection Law of the People's Republic of china-2009 for experimental animals (39,40) and were approved by the Animal care committee of People's Hospital of Rizhao. A total of 6 female BALB/c mice (average weight, 20 g; age, 4-6 weeks) were purchased from the Animal Experimental center of Jilin University and were randomly assigned to two groups: Si-SNHG14 and si-Nc.…”

Brain Tumor-Derived Extracellular Vesicles as Carriers of Disease Markers: Molecular Chaperones and MicroRNAs

“…Similarly, miR-605 has a reduced expression level in GMB tissues and cell lines, and this was correlated with patients' poor survival [153]. Conversely, increased levels of miR-605 inhibited cancer cell proliferation and growth in vitro and in vivo, by directly targeting SOX9 (SRY-box 9) and by inhibiting the activation of the PI3K (phosphatidylinositol 3-kinase)/Akt (protein kinase B) pathway [153] (Table 2).…”