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Polygonatum odoratum lectin promotes BECN1 expression and induces autophagy in malignant melanoma by regulation of miR1290

Autophagy is not only a survival response to growth-factor or nutrient deprivation but also an important mechanism for tumor-cell suicide, including melanoma. Polygonatum odoratum lectin (POL) displays apoptosis- and autophagy-inducing effects in many human tumors. POL also inhibits the growth of me...

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Detalles Bibliográficos
Autores principales: Luan, Wenkang, Qian, Yao, Ni, Xin, Chanda, Tonmoy Kumar, Xia, Yun, Wang, Jinlong, Yan, Yulan, Xu, Bin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5604572/
https://www.ncbi.nlm.nih.gov/pubmed/29066911
http://dx.doi.org/10.2147/OTT.S147406
Descripción
Sumario:Autophagy is not only a survival response to growth-factor or nutrient deprivation but also an important mechanism for tumor-cell suicide, including melanoma. Polygonatum odoratum lectin (POL) displays apoptosis- and autophagy-inducing effects in many human tumors. POL also inhibits the growth of melanoma cells, but its role and molecular mechanism in malignant melanoma remain unclear. In this study, we found that POL suppressed proliferation and induced autophagy in melanoma cells. miR1290 was upregulated and inhibited autophagy in melanoma. BECN1 is the direct functional effector of miR1290. Furthermore, we found that POL promoted BECN1 expression though inhibition of miR1290, thus inducing melanoma-cell autophagy. This finding elucidates a new role and mechanism for POL in melanoma, and provides a potential antineoplastic agent for melanoma treatment.