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

机译:玉竹凝集素通过调节miR1290促进BECN1表达并诱导恶性黑色素瘤自噬

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摘要

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.
机译:自噬不仅是对生长因子或营养缺乏的生存反应,而且是包括黑素瘤在内的肿瘤细胞自杀的重要机制。玉竹凝集素(POL)在许多人类肿瘤中均显示出凋亡和自噬诱导作用。 POL也抑制黑色素瘤细胞的生长,但在恶性黑色素瘤中的作用和分子机制仍不清楚。在这项研究中,我们发现POL抑制黑素瘤细胞的增殖并诱导自噬。 miR1290在黑色素瘤中上调并抑制自噬。 BECN1是miR1290的直接功能效应子。此外,我们发现POL通过抑制miR1290促进了BECN1表达,从而诱导黑色素瘤细胞自噬。该发现阐明了POL在黑素瘤中的新作用和机制,并为黑素瘤治疗提供了潜在的抗肿瘤药。

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