Poulsen Albrechtsen (gendercub1)

1 receptors or store-operated calcium channels.MicroRNAs (miRs) participate in the development of several cancers. miR-361-5p suppresses the proliferation of hepatocellular carcinoma (HCC) cells. However, its function and potential underlying mechanism of action in the chemoresistance of HCC remains unknown. Therefore, cisplatin (DDP)-resistant HCC cells were used to study the role and potential mechanism of action of miR-361-5p in HCC resistance to chemotherapy. TargetScan software and dual-luciferase reporter assays were used to determine whether MAPK kinase kinase 9 (MAP3K9) is a target gene of miR-361-5p. Subsequently, reverse transcription-quantitative PCR and western blot analyses demonstrated that miR-361-5p mimic decreased MAP3K9 expression levels in Huh7 cells and this change was reversed by transfection with the MAP3K9-plasmid. selleck chemicals llc In addition, compared with THLE-2 cells, miR-361-5p was downregulated, while MAP3K9 was upregulated in Huh7 cells. MAP3K9 also reversed the miR-361-5p-induced HCC cell apoptosis. A DDP-resistant cell line, Huh7/DDP, was established and MTT analysis revealed that the IC50 value of DDP treatment in Huh7/DDP cells was higher compared with that in Huh7 cells. miR-361-5p expression was lower in Huh7/DDP cells compared with that in Huh7 cells. Similarly, miR-361-5p downregulated the expression levels of MAP3K9 in Huh7/DDP cells. Furthermore, MAP3K9 reversed miR-361-5p-induced sensitivity of Huh7/DDP cells to DDP and miR-361-5p induced Huh7/DDP cell apoptosis. Therefore, the findings of the present study demonstrated that the miR-361-5p/MAP3K9 axis may serve as a new potential biomarker and therapeutic target for DDP-resistant HCC.Plantamajoside (PMS), a major component of Plantago asiatica L, has several pharmacological properties, including anti-proliferative, anti-inflammatory and anti-tumor effects. However, the effects of PMS on hepatocellular carcinoma (HCC) have yet to be determined. The aim of the present study was to investigate the effects of PMS on HCC and elucidate the underlying mechanism. All assays were conducted using 5 groups, namely control, sorafenib, and PMS 100, 50, and 25 µg/ml groups. Cell proliferation was determined by the MTT assay. Cell migration was evaluated with the wound healing and Transwell assays, respectively. Cell apoptosis and cell cycle distribution were evaluated via flow cytometry. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis and western blotting were used to further investigate the mechanism of action of PMS. Sorafenib and PMS both significantly attenuated the proliferation and migration of HCC cells, and markedly promoted cell apoptosis. PMS induced cell cycle arrest in the G0/G1 phase. The efficacy of PMS increased in a dose-dependent manner. Further study evaluated the expression of peroxisome proliferator-activated receptor (PPARγ), nuclear factor (NF)-κB and cyclooxygenase (Cox-2) using RT-qPCR analysis and western blotting. The results demonstrated that PMS promoted the expression of PPARγ and suppressed the expression of NF-κB and Cox-2. In conclusion, PMS was shown to affect cell proliferation, migration, apoptosis and cell cycle distribution. Furthermore, PMS promoted the expression of PPARγ and inhibited the expression of NF-κB and Cox-2, which may be the mechanism underlying its biological effects. Based on the results of the present study, PMS appears to be a promising agent for HCC therapy.Ischemic stroke is the most common type of stroke, and it has become a major health issue as it is characterized by high mortality and morbidity rates. Paeoniflorin (PF) is a natural compound and the main active ingredient of Radix Paeoniae. The aim of the present study was to investigate the role of PF in oxygen-glucose deprivation/reoxygenation (OGD/R)-induced injury of PC12 cells and its association with the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway. An