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首页> 外文期刊>Cell biology international. >PSPH induces cell autophagy and promotes cell proliferation and invasion in the hepatocellular carcinoma cell line Huh7 via the AMPK/mTOR/ULK1 signaling pathway
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PSPH induces cell autophagy and promotes cell proliferation and invasion in the hepatocellular carcinoma cell line Huh7 via the AMPK/mTOR/ULK1 signaling pathway

机译：PSPH通过AMPK / MTOR / ULK1信号通路诱导细胞自噬和促进肝细胞癌细胞系HUH7中的细胞增殖和侵袭

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摘要

Phosphoserine phosphatase (PSPH), a key enzyme of the l-serine synthesis pathway, has been involved in cancer progression and survival. However, limited evidence revealed the PSPH influence on hepatocellular carcinoma (HCC). Herein, we observed that PSPH expression was upregulated in both HCC tissues and cell lines, which was determined by western blotting. TCGA database showed that the PSPH protein levels were significantly upregulated and affected patient survival rates in HCC. Then gain- and loss-of-function manipulations were performed by transfection with a pcDNA-PSPH expression vector or a specific short interfering RNA against PSPH in Huh7 cells. Huh7 cell proliferation, stemness, invasion, and apoptosis were assessed by using CCK-8 test, colony formation assay, Transwell assay, and Flow cytometry analysis, respectively, and levels of autophagy-related proteins were detected by using western blotting. The results showed that PSPH could induce Huh7 cell autophagy, promote cell proliferation and invasion, and inhibit apoptosis. The knockdown of PSPH could inhibit Huh7 cell proliferation, invasion, and autophagy. Furthermore, PSPH activated Liver kinase B1 (LKB1) and TGF beta-activated kinase 1 (TAK1), affected the adenosine 5 '-monophosphate-activated protein kinase (AMPK)/mTOR/ULK1 signaling pathway, but could not activate calcium/calmodulin-dependent protein kinase kinase (CaMKK) in Huh7 cells. Inhibition of either LKB1, TAK1, or AMPK could eliminate the effect of PSPH overexpression on Huh7 cell behaviors. However, inhibition of CaMKK could not influence the effect of PSPH overexpression on Huh7 cell behaviors. In conclusion, PSPH could induce autophagy, promote proliferation and invasion, and inhibit apoptosis in HCC cells via the AMPK/mTOR/ULK1 signaling pathway.
机译：磷酸丝氨酸磷酸酶（PSPH）是l-丝氨酸合成途径的关键酶，参与了癌症的进展和生存。然而，有限的证据表明PSPH对肝细胞癌（HCC）有影响。在此，我们观察到PSPH在HCC组织和细胞系中的表达均上调，这是通过western blotting确定的。TCGA数据库显示，PSPH蛋白水平显著上调，并影响HCC患者的生存率。然后通过在Huh7细胞中转染pcDNA-PSPH表达载体或针对PSPH的特异性短干扰RNA来进行功能获得和功能丧失操作。分别通过CCK-8试验、集落形成试验、Transwell试验和流式细胞术分析评估Huh7细胞的增殖、干细胞、侵袭和凋亡，并通过western blotting检测自噬相关蛋白的水平。结果表明，PSPH能诱导Huh7细胞自噬，促进细胞增殖和侵袭，抑制细胞凋亡。敲除PSPH可抑制Huh7细胞增殖、侵袭和自噬。此外，PSPH激活的肝激酶B1（LKB1）和TGF-β激活的激酶1（TAK1）影响5'-单磷酸腺苷激活的蛋白激酶（AMPK）/mTOR/ULK1信号通路，但不能激活Huh7细胞中的钙/钙调素依赖的蛋白激酶激酶（CaMKK）。抑制LKB1、TAK1或AMPK均可消除PSPH过度表达对Huh7细胞行为的影响。然而，抑制CaMKK不能影响PSPH过度表达对Huh7细胞行为的影响。综上所述，PSPH可通过AMPK/mTOR/ULK1信号通路诱导肝癌细胞自噬，促进细胞增殖和侵袭，抑制细胞凋亡。

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