LHX2 promotes malignancy and inhibits autophagy via mTOR in osteosarcoma and is negatively regulated by miR-129-5p
LHX2 promotes malignancy and inhibits autophagy via mTOR in osteosarcoma and is negatively regulated by miR-129-5p
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LHX2 在骨肉瘤中通过 mTOR 促进恶性肿瘤并抑制自噬，并受到 miR-129-5p 的负调控。
DOI：
10.18632/aging.102427
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发表时间：
2019-11-15
期刊：
影响因子：
5.2
通讯作者：
Liu, Zhili
中科院分区：
文献类型：
--
作者：
Song, Honghai;Liu, Jiaming;Liu, Zhili
转录因子 LHX2 在许多癌症中失调，但其在骨肉瘤 (OS) 中的作用仍不清楚。在这项研究中，我们证实 LHX2 在骨肉瘤中表达上调，其沉默可抑制 OS 恶性肿瘤并通过 mTOR 信号传导诱导自噬。我们进一步证明 miR-129-5p 负向调节 LHX2 并抑制 OS 的恶性表型。 LHX2过度表达可以恢复恶性表型。总之，LHX2 在 OS 中通过 mTOR 调节肿瘤发生和自噬，并受到 miR-129-5p 的负向调节。因此，靶向 miR-129-5p/LHX2/mTOR 轴代表了 OS 治疗的一种新的治疗策略。
The transcript factor LHX2 is dysregulated in many cancers but its role in osteosarcoma (OS) remains unclear. In this study, we confirm that LHX2 is up-regulated in osteosarcoma, and that its silencing inhibits OS malignancy and induces autophagy via mTOR signaling. We further demonstrate that miR-129-5p negatively regulates LHX2 and suppresses the malignant phenotypes of OS. LHX2 overexpression could restore the malignant phenotypes. In conclusion, LHX2 regulates tumorigenesis and autophagy via mTOR in OS and is negatively regulated by miR-129-5p. Targeting the miR-129-5p/LHX2/mTOR axis therefore represents a novel therapeutic strategy for OS treatment.