Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P42345 (mTOR)
 26,049 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nitidine chloride (NC) has been demonstrated to exert a tumor-suppressive function in various types of human cancers. However, the detailed mechanism of NC-mediated anti-tumor effects remains elusive. It has been reported that SIN1, a component of mTORC2 (mammalian target of rapamycin complex C2), plays an oncogenic role in a variety of human cancers. Therefore, the inhibition of SIN1 could be useful for the treatment of human cancers. In this study, we explored whether NC triggered an anti-cancer function via the inhibition of SIN1 in osteosarcoma (OS) cells. An MTT assay was performed to measure the effect of NC on the cell growth of osteosarcoma cells, and flow cytometry was used to detect the apoptotic rate of the cells after NC treatment. The expression of SIN1 was detected by western blotting. Wound-healing assay and Transwell chamber invasion assay were conducted to analyze the motility of osteosarcoma cells following NC exposure. We found that exposure to NC led to the inhibition of cell growth, migration, and invasion and the induction of apoptosis. Mechanistically, we found that NC inhibited the expression of SIN1 in osteosarcoma cells. Overexpression of SIN1 abrogated the inhibition of cell growth and motility induced by NC in osteosarcoma cells. Our results indicate that NC exhibits its tumor-suppressive activity via the inhibition of SIN1 in osteosarcoma cells, suggesting that NC could be a potential inhibitor of SIN1 in osteosarcoma.
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PMID:Nitidine Chloride Inhibits SIN1 Expression in Osteosarcoma Cells. 3084 86

Nitidine chloride (NC) has displayed anti-tumor effects in various types of cancer. However, the role of NC in human melanoma is largely unknown. This study aimed to investigate the effects of NC on melanoma cancer cells A375 and WM35 by MTT assay. Apoptosis was measured by detecting caspase-3 protein expression level and its activity. Autophagy was measured by TEM image, immunostaining and immunoblotting assays. MTT assays showed that NC significantly blocks melanoma cells proliferation. Immunoblotting and caspase-3 activity assays showed that NC inhibited melanoma cells proliferation by inducing cell apoptosis. TEM, immunostaining and immunoblotting assays showed that NC also triggers melanoma cells autophagy and activation of the AMPK-mTOR pathway, which plays an important role in autophagy initiation. Finally, we found that blocking autophagy by 3-MA or AMPK pathway inhibitor greatly enhanced NC-induced apoptosis and cell death, indicating that NC-induced autophagy may have a cytoprotective effect in melanoma cells. Together, these results suggested that NC has strong anti-tumor effects on melanoma cells.
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PMID:Nitidine chloride efficiently induces autophagy and apoptosis in melanoma cells via AMPK-mTOR signaling pathway. 3279 70