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PLEK同源结构域家族 A 成员 3 是一个受 miR-19a-3p 调控的基因,通过下调 Akt 通路抑制骨肉瘤的肿瘤生长。

Pleckstrin homology-like domain family A, member 3, a miR-19a-3p-regulated gene, suppresses tumor growth in osteosarcoma by downregulating the Akt pathway.

机构信息

Department of Orthopedics, The Second Affiliated Hospital, Dalian Medical University, Dalian, China.

Department of Orthopedic Surgery, The Third People's Hospital of Dalian, Non-directly Affiliated Hospital of Dalian Medical University, Dalian, China.

出版信息

Bioengineered. 2022 Feb;13(2):3993-4009. doi: 10.1080/21655979.2022.2031404.

DOI:10.1080/21655979.2022.2031404
PMID:35112982
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8974154/
Abstract

Pleckstrin homology-like domain family A, member 3 (), is emerging as a critical regulator for multiple cancers. Nevertheless, the expression and role of in osteosarcoma remain unknown. Herein, we purposed to elucidate the role of in the progression and chemoresistance of osteosarcoma. According to the bioinformatics analysis, expression was low in osteosarcoma patients, and low content was linked to poor prognosis. Additionally, activation of suppressed osteosarcoma cell proliferation, migration, and chemoresistance, whereas inhibition caused the opposite effects. Mechanistically, our data revealed that negatively regulates the Akt/GSK3β signaling cascade in osteosarcoma. Furthermore, we found that miR-19a-3p might exert its oncogenic function by inhibiting expression in osteosarcoma. These results demonstrated miR-19a-3p/ / Akt/GSK3β axis has a pivotal role in osteosarcoma, and is a prospective therapeutic target for treating osteosarcoma.

摘要

PH domain and leucine-rich repeat protein phosphatase 3 () 是一种肿瘤抑制因子,在多种癌症中发挥重要作用。然而,其在骨肉瘤中的表达和作用尚不清楚。本研究旨在探讨在骨肉瘤发生发展及耐药中的作用。生物信息学分析显示,在骨肉瘤患者中低表达,低表达与不良预后相关。此外,激活可抑制骨肉瘤细胞增殖、迁移和耐药性,而抑制则产生相反的效果。机制研究表明,通过负调控 Akt/GSK3β 信号级联在骨肉瘤中发挥作用。此外,我们发现 miR-19a-3p 可能通过抑制在骨肉瘤中的表达发挥致癌作用。这些结果表明 miR-19a-3p//Akt/GSK3β 轴在骨肉瘤中具有重要作用,是治疗骨肉瘤的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8d6/8974154/7ff5d40b053e/KBIE_A_2031404_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8d6/8974154/c83c0130b171/KBIE_A_2031404_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8d6/8974154/f7a18f1ceac8/KBIE_A_2031404_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8d6/8974154/a99a2f2d27f0/KBIE_A_2031404_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8d6/8974154/90ecfb3e6db5/KBIE_A_2031404_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8d6/8974154/f3859f6ad296/KBIE_A_2031404_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8d6/8974154/774cc45e319c/KBIE_A_2031404_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8d6/8974154/e9b8481f4a0c/KBIE_A_2031404_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8d6/8974154/4a45f6d55d14/KBIE_A_2031404_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8d6/8974154/7ff5d40b053e/KBIE_A_2031404_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8d6/8974154/c83c0130b171/KBIE_A_2031404_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8d6/8974154/f7a18f1ceac8/KBIE_A_2031404_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8d6/8974154/a99a2f2d27f0/KBIE_A_2031404_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8d6/8974154/90ecfb3e6db5/KBIE_A_2031404_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8d6/8974154/f3859f6ad296/KBIE_A_2031404_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8d6/8974154/774cc45e319c/KBIE_A_2031404_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8d6/8974154/e9b8481f4a0c/KBIE_A_2031404_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8d6/8974154/4a45f6d55d14/KBIE_A_2031404_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8d6/8974154/7ff5d40b053e/KBIE_A_2031404_F0008_OC.jpg

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