Ovarian cancer is one of the most common causes of death from gynecologic tumors and is an important public health issue. Ghrelin is a recently discovered bioactive peptide that acts as a natural endogenous ligand of the growth hormone secretagogue receptor (GHSR). Several studies have identified the protective effects of ghrelin on the mammalian reproductive system. However, little research has been done on the effects of ghrelin on ovarian cancer cells, and the underlying mechanisms of these effects. We sought to understand the potential involvement of mitogen-activated protein kinases (MAPKs) in ghrelin-mediated inhibition of growth of the ovarian line HO-8910. We applied different concentrations of ghrelin and an inhibitor of the ghrelin receptor (D-Lys3-GHRP-6) to HO-8910 cells and observed the growth rate of cells and changes in phosphorylation of the MAPKs ERK1/2, JNK and p38. We discovered that ghrelin-induced apoptosis of HO-8910 cells was though phosphorylated ERK1/2, and that this phosphorylation (as well as p90rsk phosphorylation) was mediated by the GHSR. The ERK1/2 pathway is known to play an essential part in the ghrelin-mediated apoptosis of HO-8910 cells. Hence, our study suggests that ghrelin inhibits the growth of HO-8910 cells primarily through the GHSR/ERK pathway.

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The current study was designed to evaluate the aqueous extract of Terminalia chebula activity, and the main pathway was detected on lung cancer by extracts of T. chebula. Aqueous extract of T. chebula was separated using a zeolite, and five fractions of T. chebula extract were obtained and analyzed by ultraviolet (UV) and infrared (IR) spectroscopy. Antiproliferative activity was evaluated by 3- (4,5-dimethylthiazol-2-yl

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The activation of phase-specific cyclin-dependent kinases is associated with ordered cell cycle transitions. Among the mammalian Cdks, Cdk2 is essential for liver cancer cell proliferation. The related cycling protein CDK2 was analyzed by 2D-gel and MALDI-TOF/TOF MS mass assay in liver cancer cells, which CDK2 was silenced. The results showed four significantly different spots in cell ribonucleoprotein (similar to ribosomal protein S12, chaperonin 10-related protein, beta-actin and zinc finger protein 276) and four in plasmosin (aldolase A protein, hCG, anonymous protein and tubulin, gamma complex associated protein 2). In the plasmosin, aldolase A catalyzes the production of tublin and actin. Together they regulate the cell cycle and arrest the cell in the S phage. In the cell ribonucleoprotein, proteins with homology to ribosomal protein S12 and chaperonin 10 play a similar role in cell cycle regulation.

ObjectiveTo explore the autophagy effect of ghrelin on the ovarian cancer cell line SK-OV-3. And the lncRNA which regulate the ghrelin effect SK-OV-3 autophagy was showed.Methodsthe expression of ghrelin in the ovarian cancer tissues was analyzed according GEPIA database and HPA database. The CCK-8 was used to detect the the optimal concentration of ghrelin effect on the SK-OV-3. The influence on the SK-OV-3 cell autophagy by ghrelin was showed by detecting the expression of Beclin-1, LC3Ⅰand LC3Ⅱusing western blot. Linc00598 selected as the effecting the SK-OV-3 cells autophagy by ghrelin using RNA-Seq. And the Linc00598 which was silenced or overexressed promote the SK-OV-3 cells autophagy treated by ghrelin though western blot.ResultsGhrelin was expressed low in the ovarian cancer tissues. Ghrelin concentratio of 600 ng/ml was the optimal concentration o and 24 h was the optimal time. Ghrelin can promote the SK-OV-3 cell autophagy. Ghrelin mainly through linc00598 to promote the SK-OV-3 cells autophagy. When the linc00598 silenced, ghrelin promote SK-OV-3 cells autophagy was inhibited. And When the linc00598 overexpressed, ghrelin promote SK-OV-3 cells autophagy was inhanced.ConclusionsGhrelin promote SK-OV-3 cells autophagy. Additionally, we proved that ghrelin regulated the progression of SK-OV-3 cells autophagy by linc00598/ Beclin1 axis.

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