Knockdown of long non-coding RNA CDKN2B-AS1 suppresses the progression of breast cancer by miR-122-5p/STK39 axis.

The lncRNAs have been made certain to take part in the development of most cancers in multiple ways. Here, our purpose is to making observation of the biological role and function of lncRNA CDKN2B-AS1 in human breast cancer. Twenty-eight pairs of breast cancer tissue and adjacent normal tissue from breast cancer patients were used to investigate the expression of CDKN2B-AS1 by qRT-PCR. And a lentivirus-shRNA guided CDKN2B-AS1 were to reduce its expression. The function of CDKN2B-AS1 was analyzed using a series of in vitro assays. Meanwhile, the xenograft model was used to further explicate the role of CDKN2B-AS1 in breast cancer. As for the results, there is a relative rich expression of CDKN2B-AS1 in breast cancer tissues compared with the corresponding adjacent normal tissues. Compared with the human breast epithelial cell line, the abundant expression of CDKN2B-AS1 in breast cancer cells were revealed as well. Then, knockdown CDKN2B-AS1 inhibited the malignant biological behaviors of MCF7 and T47D cells. In mechanism, CDKN2B-AS1 sponged the miR-122-5p to regulate STK39 expression. Furthermore, the inhibition effect with sh-CDKN2B-AS1 on breast cancer cells was alleviated by miR-122-5p inhibitor. Last, an in vivo model also confirmed that knockdown CDKN2B-AS1 retarded the growth of breast cancer. Our data concluded that knockdown of CDKN2B-AS1 suppresses the progression of breast cancer by miR-122-5p/STK39 axis.

LncRNA AFAP-AS1 promotes anaplastic thyroid cancer progression by sponging miR-155-5p through ETS1/ERK pathway.

Anaplastic thyroid cancer (ATC) is the most common malignant endocrine tumors which resist to majority treatment. Thus, there is impelling need to figure out the mechanism of progress of ATC. In this study, we explored the function and mechanism of lncRNA actin filamentin-1 antisense RNA (AFAP-AS1) which provided a new biomarker for ATC. Viabilities and apoptosis were tested by CCK-8, colony formation and flow cytometry. The interactions between miR-155-5p and AFAP-AS1 or ETS1 was detected by luciferase reporter assays. ETS proto-oncogene1/mitogen-activated protein kinase1 (ETS1/ERK) pathway was assessed by Western blot. Xenograft models were built to confirm the function of AFAP-AS1 in vivo. Firstly, we showed that relative RNA expression of AFAP-AS1 in ATC cells was higher than in immortalized thyroid cells. Next, AFAP-AS1 was verified as an oncogene in ATC since knock-down of AFAP-AS1 inhibited cell proliferation and accelerated apoptosis. In addition, miR-155-5p was negatively regulated by AFAP-AS1. Moreover, AFAP-AS1 regulated ETS1/ERK pathway by sponging miR-155-5p. Finally, we confirmed knock-down of AFAP-AS1 significantly suppressed tumor proliferation in vivo. Our research proved that AFAP-AS1 could facilitate progression of thyroid cancer sponging miR-155-5p through ETS1/ERK pathway.

Naringenin Prevents Propofol Induced Neurodegeneration in Neonatal Mice Brain and Long-Term Neurocognitive Impacts on Adults.

BACKGROUND: Natural products have shown neuroprotective effects in neurodegenerative conditions. Naringenin is a natural flavonoid with various pharmacological activities especially antioxidant, anti-inflammatory and neuroprotective properties. We investigated the effects of naringenin on anesthetic propofol-induced impacts on neonatal mouse brain development and consequent long-term neurocognitive impacts during adulthood. MATERIALS AND METHODS: Female C57Bl/6 and male CD-1 mice and postnatal day 7 (P7) pups were exposed to propofol (2.5 mg/kg) and propofol with naringenin (50 mg/kg). Mice pups were allowed to grow until week 10 (adulthood), and memory and learning were assessed. RESULTS: Propofol caused neurodegeneration by inducing apoptosis in the neonatal mouse brains while naringenin administration prevented neuronal cell loss by preventing neuronal apoptosis in neonatal mouse brains. Propofol caused degenerative alterations in metabolic factors pH, PO2, glucose and lactate, which were subsequently restored by naringenin treatment. Propofol-exposed mice, when developed into adults, showed long-term neuronal deficits, impaired neurocognitive functions, and memory and learning restrictions. CONCLUSION: Administration of naringenin to propofol-exposed mice resulted in significant neuroprotective effects by restoring long-term neurocognitive functions. The molecular mechanism behind the effects of naringenin was mediated by suppressing apoptosis and preventing cellular inflammation. These findings suggest that propofol administration requires careful consideration and that naringenin may prevent neurodegeneration and neurocognitive functions.

Effect of paeonol on antioxidant and immune regulatory activity in hepatocellular carcinoma rats.

The study investigated the immunity and antioxidant potential of paeonol by employing a hepatocellular carcinoma (HCC) rat model. Three doses of paeonol (20, 40, 60 mg/kg b.w. orally) were administrated to diethylnitrosamine (DEN)-induced HCC rats. Results showed that paeonol significantly reduced the serum AST, ALT, ALP, GGT, AFU and liver MDA levels, increased serum WBC, TP, ALB, A/G, TNF-α and IFN-γ and liver antioxidant enzymes activities (SOD, CAT, GSH-Px, GR) in HCC rats. Altogether, these results suggest that the paeonol could effectively decrease oxidative injury and improve immunity function in HCC rats.

Evaluation of antitumour activity of tea carbohydrate polymers in hepatocellular carcinoma animals.

Box-Behnken design criterion was applied to identify the significant effects of various extraction parameters such as temperature, time, and solvent-solid ratio on extraction of tea carbohydrate. Among the three variables tested extraction temperature, and solvent-solid ratio were found to have significant effect on tea carbohydrate extraction. The most suitable condition for extraction of tea carbohydrate was found to be a single step extraction at extraction temperature 90°C, extraction time 30 min, and solvent-solid ratio 5:1. At these optimum extraction parameters, the maximum yield of tea carbohydrate obtained experimentally was found to be very close to its predicted value of 3.47% dry weight of root. Then, we have studied the influence of tea carbohydrate on biochemical parameters in hepatocellular carcinoma (HCC) animals. Hepatocellular carcinoma was induced by the injection of 1×10(5) H22 hepatocarcinoma cells into right hind thigh muscle in experimental animals. Tea carbohydrate could inhibit tumour growth and decrease microvessel density in tumour tissue. The altered amount of serum white blood cells (WBC), Interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α) in HCC animals were dose-dependently increased, whereas activities of serum alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase (ALP) were dose-dependently decreased in the drug treated animals. In addition, tea carbohydrate administration could decrease expression of vascular endothelial growth factor (VEGF) and proliferating cell nuclear antigen (PCNA) in H22 tumor tissue. It can be concluded that tea carbohydrate displayed strong antitumour activity in animals.