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首页> 美国卫生研究院文献>Cancer Medicine >Exosome–transmitted microRNA‐133b inhibited bladder cancer proliferation by upregulating dual‐specificity protein phosphatase 1
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Exosome–transmitted microRNA‐133b inhibited bladder cancer proliferation by upregulating dual‐specificity protein phosphatase 1

机译：透过的微小RNA-133B通过上调双特异性蛋白磷酸酶1抑制膀胱癌增殖

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Bladder Cancer (BC) is the ninth most common tumor in the world and one of the most common malignant tumors of the urinary system. Some studies reported that miR‐133b expression is reduced in BC, but whether it plays a role in the development of BC and its mechanism is unclear. microRNAs can be packaged into exosomes to mediate communication between tumor cells, affecting their proliferation and apoptosis. The objective of this study was to investigate the effect of exosomal miR‐133b on BC proliferation and its molecular mechanism. Firstly, the expression of miR‐133b was evaluated in BC and adjacent normal tissues, as well as in serum exosomes of BC patients and healthy controls. Then the delivery and internalization of exosomes in cells was observed through fluorescence localization. Cell viability and apoptosis were assessed in BC cells transfected with mimics and incubated with exosomes. The role of exosomal miR‐133b was also analyzed in nude mice transplant tumors. Furthermore, the target gene of miR‐133b was predicted through bioinformatics. The level of miR‐133b was significantly decreased in BC tissues and in exosomes from serum of patients, which was correlated with poor overall survival in TCGA. Exosomal miR‐133b could be obtained using BC cells after transfection with miR‐133b mimics. The miR‐133b expression increased after incubation with exosomal miR‐133b, which lead to the inhibition of viability and increase of apoptosis in BC cells. Exosomal miR‐133b could suppress tumor growth in vivo. In addition, we found that exosomal miR‐133b may play a role in suppressing BC proliferation by upregulating dual‐specificity protein phosphatase 1 (DUSP1). These findings may offer promise for new therapeutic directions of BC.
机译：膀胱癌（BC）是世界上最常见的肿瘤，以及泌尿系统中最常见的恶性肿瘤之一。一些研究报告说，在BC中，MIR-133B表达减少，但它在BC的发展中发挥作用，其机制尚不清楚。微小RNA可以包装成外泌体，以介导肿瘤细胞之间的沟通，影响其增殖和细胞凋亡。本研究的目的是探讨外泌体miR-133b对BC增殖及其分子机制的影响。首先，在BC和相邻的正常组织中评估miR-133b的表达，以及BC患者的血清外泌体和健康对照。然后通过荧光定位观察细胞中外肌肉的递送和内化。在用模拟物转染的BC细胞中评估细胞活力和细胞凋亡，并与外泌体孵育。外泌体miR-133b的作用也分析在裸鼠移植肿瘤中。此外，通过生物信息学预测miR-133b的靶基因。在BC组织中和来自患者血清的外泌体的MIR-133B水平显着降低，与TCGA的整体存活差相关。在用miR-133b模拟后转染后，可以使用BC细胞获得外泌体miR-133b。与外泌体miR-133b一起孵育后MiR-133b表达增加，这导致BC细胞中抑制活力和凋亡的增加。外泌体miR-133b可以抑制体内肿瘤生长。此外，我们发现外泌体miR-133b可以通过上调双特异性蛋白磷酸酶1（Dusp1）来发挥抑制BC增殖的作用。这些调查结果可以为BC的新治疗方向提供承诺。

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