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长链非编码RNA磷酸酶和张力蛋白同源物假基因1通过磷酸肌醇3-激酶/蛋白激酶B信号通路抑制骨肉瘤细胞生长。

Long non-coding RNA phosphatase and tensin homolog pseudogene 1 suppresses osteosarcoma cell growth via the phosphoinositide 3-kinase/protein kinase B signaling pathway.

作者信息

Yan Bin, Wubuli Aikepaer, Liu Yidong, Wang Xin

机构信息

Department of Orthopaedics, The Second Affiliated Hospital of Xinjiang Medical University, Urumchi, Xinjiang 830028, P.R. China.

Department of Orthopaedics, North Hospital of People's Hospital of Xinjiang Uygur Autonomous Region, Urumchi, Xinjiang 830011, P.R. China.

出版信息

Exp Ther Med. 2018 Jun;15(6):4829-4837. doi: 10.3892/etm.2018.6021. Epub 2018 Apr 2.

DOI:10.3892/etm.2018.6021
PMID:29805503
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5952087/
Abstract

Osteosarcoma is a common type of human carcinoma, which exhibits a high metastasis and recurrence rate. Previous studies have indicated that long non-coding RNA phosphatase and tensin homolog pseudogene 1 (lnPTENP1) has tumor suppressive action by modulating PTEN expression in different types of tumor cells. However, the potential mechanism by which lnPTENP1 has an effect in osteosarcoma cells remains elusive. In the present study, the role of lnPTENP1 in osteosarcoma cells was investigated and the possible mechanisms by which it functions were explored. It was revealed that lnPTENP1 transfection significantly inhibited osteosarcoma cell growth, proliferation, migration and invasion. LnPTENP1 transfection also significantly promoted apoptosis in Mg63 cells treated with tunicamycin. Further analysis revealed that lnPTENP1 transfection regulated osteosarcoma cell growth via the PI3K/AKT signaling pathway. assays revealed that lnPTENP1 transfection significantly inhibited osteosarcoma tumor growth and significantly increased the protein expression and phosphorylation levels of PI3K and AKT. In conclusion, the results of the present study indicated that lnPTENP1 may inhibit osteosarcoma cell growth via the PI3K/AKT signaling pathway, which may be a potential novel target for human osteosarcoma therapy.

摘要

骨肉瘤是一种常见的人类癌症，具有高转移率和复发率。先前的研究表明，长链非编码RNA磷酸酶和张力蛋白同源物假基因1（lnPTENP1）通过调节不同类型肿瘤细胞中的PTEN表达发挥肿瘤抑制作用。然而，lnPTENP1在骨肉瘤细胞中发挥作用的潜在机制仍不清楚。在本研究中，研究了lnPTENP1在骨肉瘤细胞中的作用，并探讨了其发挥作用的可能机制。结果显示，lnPTENP1转染显著抑制骨肉瘤细胞的生长、增殖、迁移和侵袭。lnPTENP1转染还显著促进了衣霉素处理的Mg63细胞的凋亡。进一步分析表明，lnPTENP1转染通过PI3K/AKT信号通路调节骨肉瘤细胞的生长。实验显示，lnPTENP1转染显著抑制骨肉瘤肿瘤生长，并显著增加PI3K和AKT的蛋白表达及磷酸化水平。总之，本研究结果表明，lnPTENP1可能通过PI3K/AKT信号通路抑制骨肉瘤细胞生长，这可能是人类骨肉瘤治疗的一个潜在新靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8301/5952087/923bf4917090/etm-15-06-4829-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8301/5952087/937171834cc1/etm-15-06-4829-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8301/5952087/2da94472d6b3/etm-15-06-4829-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8301/5952087/5486c2b035a9/etm-15-06-4829-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8301/5952087/b6fffb88fbc1/etm-15-06-4829-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8301/5952087/923bf4917090/etm-15-06-4829-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8301/5952087/937171834cc1/etm-15-06-4829-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8301/5952087/2da94472d6b3/etm-15-06-4829-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8301/5952087/5486c2b035a9/etm-15-06-4829-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8301/5952087/b6fffb88fbc1/etm-15-06-4829-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8301/5952087/923bf4917090/etm-15-06-4829-g04.jpg

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