Background. The aim of this study was to investigate the effect of curcumin on melanoma and its mechanism. Methods. Curcumin (0, 0.125, 0.25, or 0.5 mg/ml) was utilized to treat A375 and HT144 cell lines. The MTT analysis was used to confirm the proliferation ability. Wound healing and transwell analysis showed the migration and invasion ability. Immunofluorescence assay was used to demonstrate the effect of curcumin on SOX10 expression. Multiple bioinformatic analysis to confirm the SOX10 associated miRNA. The correlation of miR-222-3p and SOX10 was detected by Luciferase reporter assays. qRT-PCR showed the miR-222-3p level. Western blot analyzed the expression of SOX10, Notch1, and HES1 in melanoma cell treated with or without miR-222-3p inhibitor. Results. Curcumin could inhibit the proliferation, migration, and invasion of melanoma cells. Furthermore, curcumin repress the expression of SOX10, Notch1, and HES-1, and increase the expression of miR-222-3p. And the miR-222-3p could directly target to SOX10 mRNA to inhibit its expression. In addition, inhibition of miR-222-3p expression reversed the inhibitory effect of curcumin the growth of melanoma cells. Conclusion. Curcumin enhances the miR-222-3p level to reduce SOX10 expression, and ultimately inactivates the Notch pathway in repressing melanoma proliferation, migration, and invasion.
Purpose Melanoma is a serious and malignant disease worldwide. Seeking diagnostic markers and potential therapeutic targets is urgent for melanoma treatment. SOX10, a member of the SoxE family of genes, is a transcription factor which can regulate the transcription of a wide variety of genes in multiple cellular processes. Methods The mRNA level and protein expression of SOX10 is confirmed by bioinformatic analysis and IHC staining. MTT, clone formation and EdU analysis showed that SOX10 knockdown (KD) could significantly inhibit melanoma cell proliferation. FACS analysis showed that SOX10 KD could markedly enhance the level of cell apoptosis. The downstream target signaling pathway is predicted by RNA-seq based on the public GEO database. The activation of Notch signaling mediated by SOX10 is tested by qPCR and Western blot. Results Ectopic upregulation of SOX10 was found in melanoma patient tissues compared to normal nevus tissues in mRNA and protein levels. Furthermore, both mRNA and protein level of SOX10 were negatively correlated with melanoma patient’s prognosis. SOX10 knockdown could obviously suppress the proliferation ability of melanoma cells by inactivating Notch signaling pathway. Conclusion Our study confirmed that SOX10 is an oncogene and activate Notch signaling pathway, which suggests the potential treatment for melanoma patients by target SOX10/Notch axis.
Lymphoma is one of the most common malignancies of blood system, and drug resistance is an important cause of treatment failure. Multidrug resistance gene P-glycoprotein (P-gp) plays an important role in lymphoma chemotherapeutic drug resistance. Our previous studies have found that P-gp is highly expressed in doxorubicin-resistant lymphoma cells (Daudi/R). With the development of nanotechnology, a large number of nanomaterials have been applied in various biomedical fields. Therefore, in this study, P-gp inhibitor tariquidar (TAR) and chemotherapy drug doxorubicin were loaded onto gold nanoshells (AuNSs) to construct TAR-AuNSs/Dox nanodrug system. TAR and Dox were slowly released from TAR-AuNSs/Dox in an acidic tumor microenvironment. TAR-AuNSs/Dox increased the uptake of Dox by drug-resistant lymphoma cells and inhibited P-gp expression to reduce Dox pumping. Compared to the free Dox, TAR-AuNSs/Dox had a stronger killing effect on Daudi/R cells, which provided a new therapeutic strategy for the treatment of drug-resistant lymphoma.
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