Sendeng-4 is a traditional Chinese medicine that has been successfully applied to anti-inflammatory diseases in clinical practice. Monomers within Sendeng-4 showed promising antitumor activity against lung cancer, colon cancer, and cutaneous cancer. However, potency of Sendeng-4 in melanoma has not been explored. This study aims to explore the potential application of Sendeng-4 in melanoma treatment. In the present study, we systemically investigate the possibility of Sendeng-4 for treatment of melanoma cancer in vitro by proliferation assay, colony formation, flow cell cytometry, RNA-seq, western blot, and fluorescence-based assay. Our data demonstrated that Sendeng-4 suppresses the proliferation and colony formation capacity of melanoma cells and induces cell cycle block at G2/M phase and eventually cell death. Mechanistically, transcriptome sequencing demonstrates that the PI3K-AKT pathway was significantly inactivated upon Sendeng-4 exposure, which was confirmed by western blot showing decreased phosphorylation of AKT. In addition, decreased BCL-2 expression and increased BAX expression were observed, suggesting programmed cell death via apoptosis. Moreover, LC3-II production as well as autophagosomes formation was observed as demonstrated by western blot and immunofluorescence, indicating elevated autophagy network by Sendeng-4 stimulation. Collectively, we concluded that Sendeng-4 might be used as an anticancer drug for melanoma.
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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