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MicroRNA?1288 promotes cell proliferation of human glioblastoma cells by repressing ubiquitin carboxyl?terminal hydrolase CYLD expression.

ABSTRACT: Previous studies have demonstrated that microRNAs (miRs) are important regulators involved in various cancers, including human glioblastoma (GBM). However, the underlying mechanism of miR?1288 remains poorly understood, and its role in GBM has not been reported. The present study confirmed that miR?1288 expression was markedly upregulated in GBM. Ectopic expression of miR?1288 promoted the prolife-ration, colony formation and anchorage?independent growth of GBM cells. Bioinformatics analysis coupled with western blotting and luciferase report assays also indicated that miR?1288 promoted cell proliferation of GBM by targeting ubiquitin carboxyl?terminal hydrolase (CYLD). Knockdown of CYLD expression reversed the cell proliferation promotion by miR?1288?in in GBM. These results suggest that the miR?1288/CYLD axis may represent a potential therapeutic target for the treatment of GBM.

SUBMITTER: Yin J

PROVIDER: S-EPMC5865833 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature

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MicroRNA‑1288 promotes cell proliferation of human glioblastoma cells by repressing ubiquitin carboxyl‑terminal hydrolase CYLD expression.

Yin Jun J Weng Chengyin C Ma Jieke J Chen Fanfan F Huang Yecai Y Feng Mei M

Molecular medicine reports 20170913 5

Previous studies have demonstrated that microRNAs (miRs) are important regulators involved in various cancers, including human glioblastoma (GBM). However, the underlying mechanism of miR‑1288 remains poorly understood, and its role in GBM has not been reported. The present study confirmed that miR‑1288 expression was markedly upregulated in GBM. Ectopic expression of miR‑1288 promoted the prolife-ration, colony formation and anchorage‑independent growth of GBM cells. Bioinformatics analysis cou ...[more]

PMID: 28901464

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Project description:BACKGROUND:The ubiquitin-proteasome system regulate p53, caspase and Bcl-2 family proteins, and is crucial for the degradation of the defective germ cells in testes. Purpose: to evaluate the concentration of ubiquitin carboxyl-terminal hydrolase 1 (UCHL1) in the blood plasma of boys with cryptorchidism and if there is any correlation with patient age. METHODS:Patients-50 boys aged 1-4 years (median = 2,4y.) with unilateral cryptorchidism. Exclusion criteria were: previous human chorionic gonadotropin treatment, an abnormal karyotype, endocrine or immunological disorders or any long-term medication. The control group-50 healthy, age matched boys (aged 1-4 years, median = 2,1y.), admitted to the Pediatric Surgery Department for planned herniotomy. To investigate UCHL1 in blood plasma of boys with cryptorchidism, we used a novel technique Surface PLASMON RESONANCE Imaging (SPRI). RESULTS:The median concentration of UCHL1 in the blood plasma of boys with cryptorchidism, was 5-folds higher than in boys with inguinal hernia, whose testicles were located in the scrotum. We also noticed statistically significant difference between UCHL1 levels in boys with cryptorchidism up to 2 years old, and above 2 years old. Older boys, whose testicles since birth were located in the inguinal pouch or in the abdominal cavity, had higher concentration of UCHL1 in their blood plasma, than boys from younger group. In the group of cryptorchid boys, we also found slightly lower concentrations of INSL3, without statistical significance and no correlation with UCHL1 levels. CONCLUSIONS:Uchl1 concentrations in the blood plasma of boys with cryptorchidism, may reflect the heat-induced apoptosis of germ cells. Higher UCHL1 concentrations in older boys with undescended testicles, probably express intensity of germ cell apoptosis, more extensive when testicles are subjected to heat-stress for longer period. Further analyses of UCHL1 may help to elucidate its role in mechanisms influencing spermatogenesis.

Project description:Ubiquitin carboxyl-terminal hydrolase L1 (UCHL1) is a deubiquitinase known to play essential roles in the nervous tissue. Myocardial upregulation of UCHL1 was observed in human dilated cardiomyopathy and several animal models of heart disease, but the (patho)physiological significance of UCHL1 in cardiomyocytes remains undefined. Hence, we conducted this study to fill this critical gap. We produced cardiomyocyte-restricted Uchl1 knockout (CKO) by coupling the Uchl1-floxed allele with transgenic Myh6-Cre in C57B/6J inbred mice. Mice transgenic for Myh6-Cre were used as controls (CTL). Myocardial Uchl1 proteins were markedly reduced in CKO mice but they did not display discernible abnormal phenotype. Ten-week old CTL or CKO mice were subjected to left anterior descending artery ligation (myocardial infarction, MI) or sham surgery (Sham) and characterized at 7- and 28-day after surgery. Compared with Sham mice, significant increases in myocardial UCHL1 proteins were detected in CTL MI but not in CKO MI mice. MI-induced left ventricular (LV) chamber dilation, reduction of ejection fraction (EF) and fractional shortening (FS), and LV anterior wall thinning detected by echocardiography were comparable between the CTL MI and CKO MI groups 7-day post-MI. However, by 28-day post-MI, MI-induced LV chamber dilatation, EF and FS reduction, increases of myocardial ubiquitin conjugates, and increases in the heart weight to body weight ratio and the ventricular weight to body weight ratio were significantly more pronounced in CKO MI than CTL MI mice. As further revealed by LV pressure-volume relationship analyses, CKO MI mice but not CTL MI mice displayed significant decreases in stroke volume, cardiac output, and the maximum rates of LV pressure rising or declining and of LV volume declining, as well as significant increases in LV end-diastolic pressure and Tau, compared with their respective Sham controls. LC3-II flux assays reveal that autophagic flux is decreased in CKO mouse myocardium as well as in cultured Uchl1-deficient cardiomyocytes. In conclusion, UCHL1 of cardiomyocytes is dispensable for development but promotes macroautophagy in cardiomyocytes. Upregulation of UCHL1 in post-MI hearts occurs primarily in the cardiomyocytes and protects against post-MI cardiac remodeling and malfunction likely through supporting autophagic flux and proteostasis during a stress condition.

Dataset Information

MicroRNA?1288 promotes cell proliferation of human glioblastoma cells by repressing ubiquitin carboxyl?terminal hydrolase CYLD expression.

Publications

MicroRNA‑1288 promotes cell proliferation of human glioblastoma cells by repressing ubiquitin carboxyl‑terminal hydrolase CYLD expression.

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