In vitro anticancer study of novel curcumin derivatives via targeting PI3K/Akt/p53 signaling pathway.

Four new series of curcumin derivatives bearing NO-donating moiety were synthesized via etherification, nucleophilic substitution, and Knoevenagel condensation etc. The cytotoxicity activity of curcumin derivatives against five human tumor cell lines (A549, Hela, HepG2, MCF-7 and HT-29) and two normal cell lines (LO-2 and HK-2) has been studied. The results showed that compound 6a could inhibit the proliferation of MCF-7 cells remarkably and exhibit low toxicity to normal cells. Also, the underlying mechanism in vitro of compound 6a on MCF-7 was investigated. It has been found that compound 6a induced G2/M arrest and apoptosis of MCF-7 in a dose-dependent manner. Compound 6a-induced the fluorescence changes of ROS in MCF-7 cells confirmed the occurrence of apoptosis. Western Blot suggested that compound 6a decreased the expression of PI3K, as well as increased the expression of p53, cleaved caspase-9 and cleaved caspase-3. Furthermore, molecular docking revealed that compound 6a could bind well at active site of PI3K (3zim) with total score 9.59. Together, compound 6a, a potential PI3K inhibitor, may inhibit the survival of MCF-7 cells via interfering with PI3K/Akt/p53 pathway.

Long non-coding RNA BLACAT1 promotes the proliferation and invasion of glioma cells via Wnt/ß-catenin signaling.

Long non-coding RNAs (lncRNAs) are hypothesized to regulate numerous biological behaviors in human cancers. The present study aimed to explore the roles of lncRNA bladder cancer associated transcript 1 (BLACAT1) in glioma. The expression of BLACAT1 in glioma tissues and cell lines was determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). CCK-8 assay, colony formation assay, wound healing assay and Transwell invasion assay were used to explore the roles of BLACAT1 in glioma cells. RT-qPCR and western blot analysis were used to determine the BLACAT1 molecular mechanism. The findings demonstrated that lncRNA BLACAT1 was overexpressed in glioma tissues and cell lines. High BLACAT1 expression was correlated with high tumor grade in glioma patients. Functional assays determined that BLACAT1 promoted glioma cell proliferation, migration, invasion and epithelial-mesenchymal transition in vitro. In addition, it was demonstrated that BLACAT1 activated the Wnt/ß-catenin signaling pathway. In conclusion, BLACAT1 may serve as an oncogenic lncRNA in glioma progression via activation of the Wnt/ß-catenin signaling pathway. Therefore, BLACAT1 may be a novel therapeutic target for glioma treatment.

Quasi-Static Calibration Method of a High-g Accelerometer.

To solve the problem of resonance during quasi-static calibration of high-g accelerometers, we deduce the relationship between the minimum excitation pulse width and the resonant frequency of the calibrated accelerometer according to the second-order mathematical model of the accelerometer, and improve the quasi-static calibration theory. We establish a quasi-static calibration testing system, which uses a gas gun to generate high-g acceleration signals, and apply a laser interferometer to reproduce the impact acceleration. These signals are used to drive the calibrated accelerometer. By comparing the excitation acceleration signal and the output responses of the calibrated accelerometer to the excitation signals, the impact sensitivity of the calibrated accelerometer is obtained. As indicated by the calibration test results, this calibration system produces excitation acceleration signals with a pulse width of less than 1000 µs, and realize the quasi-static calibration of high-g accelerometers with a resonant frequency above 20 kHz when the calibration error was 3%.

MicroRNA-143 shows tumor suppressive effects through inhibition of oncogenic K-Ras in pituitary tumor.

MicroRNAs (miRNAs) are a class of small non-coding RNA molecules, about 21-25 nucleotides in length. Accumulating evidence demonstrated that dysregulation or dysfunction of miRNAs are involved in various diseases, including cancer. MiR-143, recently has been reported to function as an important tumor suppressor in prostate cancer, pancreatic ductal adenocarcinoma and other kinds of cancers, but rarely systematically studied in pituitary tumor. In the present study, we firstly found that miR-143 was significantly down-regulated in pituitary tumor tissues and cell lines (GH3 and MMQ). Then, subsequent studies revealed that miR-143 inhibits cell proliferation and promotes apoptosis in both GH3 and MMQ cells. In addition, K-Ras, one of the most important oncogenes involved in many kinds of cancers, was found to be suppressed by miR-143 in pituitary tumor. Furthermore, overexpression of K-Ras greatly reversed the suppressive effect of miR-143 on pituitary tumor cells. In summary, our study demonstrated that miR-143 functions as a tumor suppressor and directly targets K-Ras in human pituitary tumor.