SDF-1α/MicroRNA-134 Axis Regulates Nonfunctioning Pituitary Neuroendocrine Tumor Growth via Targeting VEGFA.
SDF-1α/MicroRNA-134 Axis Regulates Nonfunctioning Pituitary Neuroendocrine Tumor Growth via Targeting VEGFA.
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SDF-1α/MicroRNA-134 轴通过靶向 VEGFA 调节无功能垂体神经内分泌肿瘤的生长
DOI：
10.3389/fendo.2020.566761
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发表时间：
2020
影响因子：
5.2
通讯作者：
Hong Y
中科院分区：
文献类型：
--
作者：
Wang X;Fang Y;Zhou Y;Guo X;Xu K;Li C;Zhang J;Hong Y
BackgroundNonfunctioning pituitary neuroendocrine tumor (NF-PitNET) is difficult to resect. Except for surgery, there is no effective treatment for NF-PitNET. MicroRNA-134 (miR-134) has been reported to inhibit proliferation and invasion ability of tumor cells. Herein, the mechanism underlying the effect of miR-134 on alleviating NF-PitNET tumor cells growth is explored.MethodsMouse pituitary αT3-1 cells were transfected with miR-134 mimics and inhibitor, followed by treatment with stromal cell-derived factor-1α (SDF-1α) in vitro. MiR-134 expression level: we used quantitative real-time PCR (qRT-PCR) to detect the expression of miR-134. Cell behavior level: cell viability and invasion ability were assessed using a cell counting kit-8 (CCK8) assay and Transwell invasion assay respectively. Cytomolecular level: tumor cell proliferation was evaluated by Ki-67 staining; propidium iodide (PI) staining analyzed the effect of miR-134 on cell cycle arrest; western blot analysis and immunofluorescence staining evaluated tumor migration and invasive ability. Additionally, we collected 27 NF-PitNET tumor specimens and related clinical data. The specimens were subjected to qRT-PCR to obtain the relative miR-134 expression level of each specimen; linear regression analysis was used to analyze the miR-134 expression level in tumor specimens and the age of the NF-PitNET population, gender, tumor invasion, prognosis, and other indicators.ResultsIn vitro experiment, miR-134 was observed to significantly inhibit αT3-1 cells proliferation characterized by inhibited cell viability and expressions of vascular endothelial growth factor A (VEGFA) and cell cycle transition from G1 to S phase (P lt; 0.01). VEGFA was verified as a target of miR-134. Additionally, miR-134-induced inhibition of αT3-1 cell proliferation and invasion was attenuated by SDF-1α and VEGFA overexpression (P lt; 0.01). In primary NF-PitNET tumor analysis, miR-134 expression level was negatively correlated with tumor invasion (P = 0.003).ConclusionThe regulation of the SDF-1α/miR-134/VEGFA axis represents a novel mechanism in the pathogenesis of NF-PitNETs and may serve as a potential therapeutic target for the treatment of NF-PitNETs.
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影响因子：
2.8
作者：
Barbieri F;Thellung S;Würth R;Gatto F;Corsaro A;Villa V;Nizzari M;Albertelli M;Ferone D;Florio T
通讯作者：
Florio T
影响因子：
11.5
作者：
Barbieri, Federica;Bajetto, Adriana;Florio, Tullio
通讯作者：
Florio, Tullio
影响因子：
64.5
作者：
Lichtenberger, Beate M.;Tan, Poi Kiang;Sibilia, Maria
通讯作者：
Sibilia, Maria
影响因子：
3.9
作者：
Asa, S. L.;Casar-Borota, O.;Trouillas, J.
通讯作者：
Trouillas, J.
DOI：
10.1016/j.bbrc.2007.05.182
发表时间：
2007-08-03
影响因子：
3.1
作者：
Liang, Zhongxing;Brooks, Joann;Shim, Hyunsuk
通讯作者：
Shim, Hyunsuk