Objective: To investigate the changes in serum miR-124 levels in patients with acute cerebral infarction (ACI) and elucidate the underlying mechanism by a dynamic monitor.
Methods: Fifty-four patients with ACI and 51 healthy controls were included in our study. Baseline characteristics and blood samples were collected for further analysis. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to measure the serum miR-124 levels. The dual-luciferase reporter assay was used to evaluate the effect of miR-124 on iASPP, a protein that inhibits apoptosis stimulating proteins in the p53 family.
Results: Compared with normal controls, the miR-124 levels in the ACI group rapidly decreased at phase 1 (within 24?h after ischemia) (p?<?0.001) and then gradually increased at phase 2 (48?~?72?h after ischemia) (p?<?0.001) and phase 3 (the 7th day after ischemia) (p?<?0.001). The dual-luciferase reporter assay showed that miR-124 down-regulates iASPP expression in 293T cells.
Conclusion: The miR-124 levels are down-regulated in ACI patients. The dynamic changes of miR-124 might provide a possible method for the detection of ischemic stroke.
Highlights
The difference in miR-124 expression levels between ACI patients and normal controls.
Dynamic changes of miR-124 expression levels in ACI patients.
The down-regulation of miR-124 upon iASPP expression.
Objectives:To reassess the long-term camouflage effects of resin infiltration (Icon, DMG, Hamburg, Germany) of white spot lesions (WSL) and sound adjacent enamel (SAE) achieved in a previous trial. The null hypothesis was tested that there were no significantly different CIE-L*a*b*-ΔE-values between WSL and SAE areas of assessment after at least 24 months (T24) compared to those at baseline (T0).Materials and Methods:Of twenty subjects who received previous resin infiltration treatment of nteeth = 111 nonrestored, noncavitated postorthodontic WSL after multibracket treatment during a randomized controlled trial and were contacted 20 months after baseline, eight subjects (trial teeth nteeth = 40; m/f ratio 1/7; age range (mean; SD) 12–17 [15.25; 2.12] years); response rate: 40%) were available for follow-up after at least 24 months (T24). CIE-L*a*b* differences between summarized color and lightness values (ΔEWSL/SAE) of WSL and SAE were assessed using a spectrophotometer and compared to baseline data assessed prior to infiltration (T0), and those after 6 (T6), and 12 (T12) months using paired t tests at a significance level of α = 5%.Results:T24 assessments were performed after a mean 33.86 (SD: 8.64; Min: 24; Max: 45) months following T0. Mean (SD) ΔEWSL/SAE units of available teeth were 8.76 (5.33) at baseline; 5.5 (2.75) at T6; 5.2 (2.41) at T12; and 5.57 (2.6) at T24. Comparisons of T6, T12, and T24 with T0 yielded highly significant differences, whereas T6–T24 and T12–T24 differences were found to be not significant.Conclusions:Assimilation of infiltrated WSL to the color of adjacent enamel by resin infiltration is considered to be suitable for the long-term improvement in the esthetic appearance of postorthodontic WSL. 相似文献
miR-30c has been acknowledged as a tumor suppressor in various human cancers, such as ovarian cancer, gastric cancer, and prostate cancer. However, the role of miR-30c in glioblastoma (GBM) needs to be investigated.
In our study, we found that the expression of miR-30c was significantly downregulated in GBM tissues and
cell lines. We found that overexpression of miR-30c inhibited cellular proliferation of GBM cells in vitro and
in vivo. More GBM cells were arrested in the G0 phase after miR-30c overexpression. Moreover, we showed
that miR-30c overexpression suppressed the migration and invasion of GBM cells. Mechanistically, we found
that SOX9 was a direct target of miR-30c in GBM cells. Overexpression of miR-30c inhibited the mRNA
and protein levels of SOX9 in GBM cells. Moreover, there was a negative correlation between the expression
of miR-30c and SOX9 in GBM tissues. Finally, we showed that restoration of SOX9 in GBM cells reversed
the proliferation, migration, and invasion of GBM cells transfected with miR-30c mimic. Collectively, our
results demonstrated that miR-30c suppressed the proliferation, migration, and invasion of GBM cells via
targeting SOX9. 相似文献
MicroRNAs (miRNAs) have been found to be aberrantly expressed and exert essential roles in the tumorigenesis and progression of gastric cancer (GC). miR-301b-3p has been recognized as a cancer-related miRNA in lung cancer, bladder cancer and hepatocellular carcinoma. However, the function of miR-301b-3p in GC progression and its underlying mechanism have not been studied yet. In this study, we found that miR-301b-3p expression was up-regulated in GC tissues compared to adjacent noncancerous tissues. Furthermore, the elevated levels of miR-301b-3p were detected in GC cell lines (SGC-7901, AGS, MKN-45 and MGC-803) as compared with GES-1 cells. Interestingly, GC tissues from patients with tumor size ≥ 5 cm and advanced tumor stages showed obvious higher levels of miR-301b-3p compared to matched controls. Functionally, miR-301b-3p knockdown prominently inhibited cell proliferation, and induced cell cycle arrest at G1 phase and apoptosis in MGC-803 cells. Meanwhile, ectopic expression of miR-301b-3p conversely regulated these biological behaviors of MKN-45 cells. Next, we found that miR-301b-3p knockdown increased, whereas miR-301b-3p overexpression reduced the expression of zinc finger and BTB domain containing 4 (ZBTB4) in GC cells. Accordingly, luciferase reporter assay identified ZBTB4 as a direct target of miR-301b-3p. ZBTB4 overexpression markedly restrained the growth of MGC-803 cells. More importantly, ZBTB4 silencing partially reversed miR-301b-3p knockdown-induced tumor suppressive effects on MGC-803 cells. In conclusion, we firstly revealed that miR-301-3p was highly expressed in GC and contributed to tumor progression via attenuating ZBTB4, which might provide a novel molecular-targeted strategy for GC treatment. 相似文献
Non-small cell lung cancer (NSCLC) is the most common type of primary lung cancer and regarded as cancer killer. The aim of this study was to discover the detailed function and molecular mechanism of F-box and leucine rich repeat protein 3 (FBXL3) in NSCLC. In this study, the expression level of FBXL3 in NSCLC tissues and cell lines was firstly examined and identified. Moreover, the relationship between FBXL3 and the overall survival rate of NSCLC patients was analyzed by Kaplan–Meier survival curve. Functionally, MTT, colony formation assay and transwell assays were performed to determine the role of FBXL3 in regulating NSCLC cell proliferation, migration and invasion. The proliferation and migration were suppressed by overexpression of FBXL3, indicating the potential tumor suppressive role of FBXL3 in NSCLC. In addition, the dual-luciferase reporter and RNA pull-down assays revealed that miR-4735-3p was a novel upstream modulator of FBXL3. Further study showed that miR-4735-3p was upregulated in NSCLC tissues and cell lines. Finally, rescue assays and function assays revealed that miR-4735-3p exerted oncogenic function in NSCLC, and this function can be attenuated by FBXL3. Taken together, FBXL3 was regulated by miR-4735-3p and suppressed cell proliferation and invasion in non-small cell lung cancer. 相似文献