Long noncoding RNA LINC00662 functions as miRNA sponge to promote the prostate cancer tumorigenesis through targeting miR-34a.

OBJECTIVE: Mounting evidence indicates that long noncoding RNAs (lncRNAs) play a critical role in the tumorigenesis. Up-regulation of lncRNA LINC00662 (LINC00662) has previously confirmed in several tumors. However, the study of LINC00662 in prostate cancer (PCa) is limited. Hence, to determine the expression pattern and function of LINC00662 in PCa. PATIENTS AND METHODS: LINC00662 expression was first detected in PCa cell lines and tissue samples by qRT-PCR. Based on follow-up data, correlations of LINC00662 expression and clinicopathological features, including overall survival, in PCa patients were evaluated. Cell proliferation, migration, invasion, and apoptosis were detected by CCK-8 assay, colony-forming assay, Wound-healing assay, transwell assay, and flow cytometry, respectively. Additionally, LINC00662-specific miRNA was further confirmed using the dual-luciferase reporter assay and RT-PCR. RESULTS: LINC00662 was significantly upregulated in PCa tissues and cell lines compared with adjacent normal tissue and a normal prostate epithelial cell line. Higher expression of LINC00662 was positively associated with distant metastasis and shorter overall survival. In addition, multivariate analysis revealed that tissue LINC00662 expression was confirmed to be an independent prognostic factor for PCa. Furthermore, LINC00662 silencing inhibited the proliferation, migration, and invasion of PC-3 and LNCaP cells, and promoted apoptosis in vitro. Bioinformatics methods and luciferase reporter assay revealed the close link within miR-34a and 3'-untranslated region (UTR) of LINC00662 and further confirmed that LINC00662 could function as a sponge of miR-34a in PCa cells. Also, the results of RT-PCR showed that knockdown of LINC00662 suppressed the expression levels of miR-34a. CONCLUSIONS: The current results further enhanced our understanding of the effects of LINC00662 in PCa and may help to provide a new potential target for PCa treatment.

[Neurofeedback therapy in the treatment of tinnitus].

Neurofeedback therapy is a fast-growing field of tinnitus treatment, which is a new type of biofeedback therapy. In the past, the "muscle tone" and "blood flow" were used as feedback signals in biofeedback therapy to treat tinnitus, however there was no long-term follow-up report. Instead, neurofeedback therapy utilizes EEG (electroencephalogram) as the feedback signal, which is also called EEG biofeedback therapy. At present, most treatments of tinnitus only record subjective measures of patients as evaluation indicators, whereas neurofeedback therapy is more convincing for using comprehensive evaluation including changes of brain wave as objective indicators and subjective measures of patients. A significant number of tinnitus patients have varying degree of hearing loss. As neurofeedback therapy takes advantage of EEG as feedback signal that is delivered to the patients through visual information, it has unique advantages of being not affected by the degree of hearing loss compared to the sound masking or other sound treatment. Long-term follow-up results showed that the efficacy of neurofeedback therapy was stable after half a year of short-term treatment. This paper summarizes the progress of the various types of biofeedback therapy in the treatment of tinnitus, and focuses on the neurofeedback therapy for the mechanism, indication, process, efficacy evaluation, defect and prospect of neurofeedback therapy in tinnitus treatment in order to help promote the development of domestic clinical neurofeedback therapy in tinnitus.

Flow cytometer analysis of cell apoptosis of endometrial carcinoma with Wnt10b.

The aim of this study is to analyze the cell apoptosis of endometrial carcinoma (EC) with Wnt10b by Fluorescence Activated Cell Sorting (FACS) technology. AN3CA cell lines and Ishikawa-H-12 cell lines were taken as the in-vitro cell models to observe the influence of Wnt10b on key factors of Wnt signal pathway. Methyl thiazolyl tetrazolium (MTT) was applied for the detection of cell proliferation while FACS was used for the detection of cell apoptosis. Data were analyzed using statistical software SPSS14.0. After the overexpression of Wntl0b in AN3CA cells, the apoptosis rate dropped significantly compared with the two control groups (p < 0.05); while the apoptosis rate increased significantly compared with the control groups (p < 0.01) after Wntl0b knock-off in Ishikawa3-H-12 cells. In normal endometrium, Wnt10b gene expression was negative, while that in EC cells was positive. It can be concluded that Wnt10b gene can promote EC cell proliferation and inhibit its apoptosis.

Non-nuclear activation of signal transducer and activator of transcription 3 by 17ß- estradiol in endometrial cancer cells.

Why estrogen hyperstimulation can lead to endometrial carcinogenesis has not been fully clear yet. Non-nuclear action of estrogen has arised much attention of many experts. Signal transducer and activator of transcription 3 is a very important signal molecule, which plays vital role in endometrial canver. The present study is oriented to the problem whether estrogen can activate STAT3 by non-nuclear action in endometrial cancer cells. So, the levels of phosphorylated STAT3 (P-STAT3) and total STAT3 were examined by western blot in endometrial cancer cells including Ishikawa with rich-expressed estrogen receptor (ER) and HEC-1A with poor-expressed ER after stimulation with 1µM estradiol (E2) at different time points and at varied doses of E2 for optimal time. Inhibitory role of AG490 on activation of STAT3 induced by E2 was also tested. P-STAT3/STAT3 was used as a measure of activation of STAT3. We found that maximum P-STAT3/STAT3 took place at 15 min in both Ishikawa cells and HEC-1A cells. The activation of STAT3 elicited gradually with increasing doses of E2. AG490 stopped the activating STAT3 in the same dose-dependent manner in both endometrial cancer cells. The results demonstrate that E2 is able to activate STAT3 in both Ishikawa with rich-expressed ER and HEC-1A with poor-expressed ER endometrial cancer cells by non-nuclear action, which provides the preliminary laboratory basis for the probability of endometrial adenocarcinoma treatment with blockage of STAT3 signaling, especially for ER-poor endometrial adenocarcinoma.

Role of phosphate and kinetic characteristics of complete iron release from native pig spleen ferritin-Fe.

The kinetics for complete iron release showing biphasic behavior from pig spleen ferritin-Fe (PSFF) was measured by spectrophotometry. The native core within the PSFF shell consisted of 1682 hydroxide Fe3+ and 13 phosphate molecules. Inhibition kinetics for complete iron release was measure by differential spectrophotometry in the presence of phosphate; the process was clearly divided into two phases involving a first-order reaction at an increasing rate of 46.5 Fe3+/PSFF/min on the surface of the iron core and a zero-order reaction at a decreasing rate of 6.67 Fe3+/PSFF/min inside the core. The kinetic equation [C(PSFF-Fe3+)max - C(PSFF-Fe3+)t](1/2) = Tmax - Tt gives the transition time between the two rates and represents the complex kinetic characteristics. The rate was directly accelerated twofold by a mixed reducer of dithionite and ascorbic acid. These results suggest that the channel of the PSFF shell may carry out multiple functions for iron metabolism and storage and that the phosphate strongly affects the rate of iron release.