Plantamajoside (PMS) has been shown to have anticancer effects and is the main compound of Plantago asiatica. The aim of the present study was to investigate the effects of PMS on malignant melanoma and its molecular mechanisms. The malignant melanoma cell line A2058 was treated with different concentrations of PMS (0, 20, 80 and 160 µg/ml) for 24, 48 or 72 h, followed by cell viability detection using the Cell Counting Kit-8 assay. The present results suggested that PMS inhibited cell viability in a dose-dependent manner. In addition, flow cytometry was used to analyze cell apoptosis, and Transwell assays were used to investigate cell migration and invasion. The present results suggested that PMS induced A2058 cell apoptosis, and inhibited cell invasion and migration in a dose-dependent manner. In order to study the molecular mechanism by which PMS inhibited malignant melanoma growth and metastasis, reverse transcription-quantitative PCR and western blotting were used to determine the expression levels of apoptotic-related genes and PI3K/AKT signaling pathway-related proteins. The present results indicated that PMS inhibited the protein and mRNA expression of Bcl-2, and promoted the expression of Bax and caspase-3 in a dose-dependent manner. The protein expression level of phosphorylated-AKT was dose-dependently reduced by PMS treatment. Collectively, the present results suggested that PMS inhibited the invasion, migration and viability of malignant melanoma cells. In addition, PMS induced apoptosis by regulating the expression levels of apoptotic-related genes and the activation of the PI3K/AKT signaling pathway, thereby exerting anti-malignant melanoma effects.
Avicularin (AL), quercetin-3-α-L-arabinofur anoside, has various pharmacological properties such as anticancer and anti-infective effects. However, the potential molecular mechanism via which AL exerts its anticancer activity is not fully understood. Cutaneous squamous cell carcinoma (CSCC) is the second most common skin cancer, where metastasis has resulted in in effective clinical treatments. The aim of the present in vitro study was to investigate the anticancer effects and underlying mechanism of AL on human CSCC. The present results suggested that AL dose-dependently inhibited SCC13 cell viability and induced apoptosis. In addition, the present results suggested that AL induced apoptosis via repression of the mitogen-activated protein kinase kinase (MEK)/NF-κB signal pathway, thereby affecting the expression of apoptosis-related genes. Bax expression level was increased, while Bcl-2 expression level was decreased in SCC13 cells following AL treatment. In addition, the MEK/NF-κB signaling pathway-related genes p-MEK and phosphorylated-p65 were also decreased. The present results suggested that AL treatment increased the expression level of E-cadherin, but decreased the expression levels of N-cadherin, matrix metalloproteinase (MMP)-9 and vimentin in SCC13 cells. Collectively, the present results suggested that AL may have an anti-CSCC effect by inhibiting cell viability, inducing apoptosis and inhibiting epithelial-mesenchymal transition (EMT) of CSCC cells. The mechanism of these anti-CSCC effects was suggested to be via the regulation of apoptosis-related genes and EMT-related genes, and the inhibition of the MEK/NF-κB signaling pathway. Materials and methods Cell culture and treatment. DMEM (Gibco; Thermo Fisher Scientific, Inc) with 10% FBS (Gemini Bio-Products, Inc.), 10 U/ml penicillin-G and 10 mg/ml streptomycin (Gemini
Ovarian cancer is one kind of a deadly gynecological malignancy. Recent study has shown that SND1 was associated with the development of ovarian cancer. Furthermore, the expression of lncRNA XIST in ovarian cancer was down-regulated. However, it is unclear whether lncRNA XIST could affect the occurrence and development of ovarian cancer by targeting SND1. In this study, we used the lentivirus to establish the overexpression and knockdown SND1 ovarian cancer cells. And we next detected the proliferation and invasion of these cells in diverse groups. Then, the luciferase assays were performed to detect the targeted effect of lncRNA XIST on SND1 and determined the expression of SND1 in the overexpressed lncRNA XIST ovarian cancer cells. We found that SND1 promoted the proliferation and invasion of ovarian cancer cells. And the lncRNA XIST targeted and suppressed the expression of SND1. Overexpression of lncRNA XIST inhibited the proliferation and invasion of ovarian cancer cells. However, the overexpression of SND1 alleviated the inhibitory efficacy of lncRNA XIST on the proliferation and invasion of ovarian cancer cells. LncRNA XIST inhibited the proliferation and invasion of ovarian cancer by suppressing the expression of SND1.
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