Adipose-derived stem cell-derived extracellular vesicles inhibit neuroblastoma growth by regulating GABBR1 activity through LINC00622-mediated transcription factor AR,Journal of Leukocyte Biology

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Adipose-derived stem cell-derived extracellular vesicles inhibit neuroblastoma growth by regulating GABBR1 activity through LINC00622-mediated transcription factor AR
Journal of Leukocyte Biology ( IF 3.6 ) Pub Date : 2021-08-27 , DOI: 10.1002/jlb.1mia0321-164r
Mengguo Guo ₁ , Dongpeng Li ₁ , Yawen Feng ₁ , Mu Li ₁ , Bo Yang ₁

Affiliation

Neuroblastoma (NB) is a huge threat to children's health. Adipose-derived stem cells-derived extracellular vesicles (ADSC-Evs) can regulate tumor progression. This study aimed to identify the role of ADSC-Evs in NB. Following ADSC-Ev isolation and identification, PKH26-labeled ADSC-Evs were cocultured with NB cells to observe the internalization of ADSC-Evs. ADSC-Ev effects on NB cell proliferation, invasion, and migration were assessed. The regulatory molecules related to NB development were predicted. The expressions of and relations among LINC00622, transcriptional factor androgen receptor (AR), and gamma-aminobutyric acid B-type receptor 1 (GABRR1) were detected and verified. LINC00622 was inhibited in ADSCs to evaluate ADSC-Ev effects on NB cells. Xenograft tumor experiment in nude mice was further performed to evaluate the effects of ADSC-Evs-carried LINC00622 on NB in vivo. ADSC-Evs inhibited NB cell proliferation, invasion, and migration. ADSC-Evs increased GABBR1 expression in NB cells. ADSC-Evs-carried LINC00622 mediated AR to promote GABBR1 expression. Silencing LINC00622 in ADSCs weakened the inhibition of ADSC-Evs on NB cell malignant behaviors. ADSC-Evs reduced tumor growth in nude mice, which was restored after inhibiting LINC00622 expression in ADSCs. We highlighted that ADSC-Evs carried LINC00622 into NB cells to inhibit transcription factor AR and promote GABBR1 expression, thus inhibiting NB cell growth.

中文翻译：

脂肪干细胞来源的细胞外囊泡通过 LINC00622 介导的转录因子 AR 调节 GABBR1 活性来抑制神经母细胞瘤生长

神经母细胞瘤（NB）对儿童的健康构成巨大威胁。脂肪干细胞衍生的细胞外囊泡（ADSC-Evs）可以调节肿瘤进展。本研究旨在确定 ADSC-Evs 在 NB 中的作用。 ADSC-Ev分离鉴定后，将PKH26标记的ADSC-Ev与NB细胞共培养，观察ADSC-Ev的内化情况。评估了 ADSC-Ev 对 NB 细胞增殖、侵袭和迁移的影响。预测了与NB发育相关的调控分子。检测并验证LINC00622、转录因子雄激素受体（AR）、γ-氨基丁酸B型受体1（GABRR1）的表达及相互关系。在 ADSC 中抑制 LINC00622，以评估 ADSC-Ev 对 NB 细胞的影响。进一步进行裸鼠异种移植瘤实验，评价ADSC-Evs携带的LINC00622对体内NB的影响。 ADSC-Evs 抑制 NB 细胞增殖、侵袭和迁移。 ADSC-Evs 增加 NB 细胞中 GABBR1 的表达。 ADSC-Evs 携带 LINC00622 介导 AR 促进 GABBR1 表达。沉默ADSCs中的LINC00622减弱了ADSC-Evs对NB细胞恶性行为的抑制作用。 ADSC-Evs 减少了裸鼠体内的肿瘤生长，抑制 ADSC 中的 LINC00622 表达后，肿瘤生长得以恢复。我们强调，ADSC-Evs 将 LINC00622 携带到 NB 细胞中，抑制转录因子 AR 并促进 GABBR1 表达，从而抑制 NB 细胞生长。

更新日期：2021-08-27

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