PTTG1通过诱导c-myc参与TNF-α相关的肝细胞癌。,Cancer Medicine

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PTTG1通过诱导c-myc参与TNF-α相关的肝细胞癌。
Cancer Medicine ( IF 2.9 ) Pub Date : 2019-08-06 , DOI: 10.1002/cam4.2473
Xianyi Lin ₁ , Yidong Yang ₁ , Yunwei Guo ₁ , Huiling Liu ₁ , Jie Jiang ₁ , Fengping Zheng ₁ , Bin Wu ₁

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肝细胞癌（HCC）是由多种因素引起的恶性疾病。然而，在肝癌中的基因组和分子畸变在很大程度上是未知的。在这里，垂体肿瘤转化基因1（PTTG1）被发现为肝癌中潜在的炎症相关癌基因，并对其功能和分子机制进行了研究。mRNA表达芯片，实时聚合酶链反应（PCR），免疫组织化学和免疫印迹分析表明PTTG1在HCC中被上调。进一步的体外和体内研究表明，促炎细胞因子肿瘤坏死因子-α（TNF-α）诱导PTTG1表达，并且发现PTTG1上调c-myc（一种著名的癌基因）。PTTG1的下调减少c-myc和增殖细胞核抗原（PCNA）的表达并抑制细胞增殖。有趣的是，10058-F4对c-myc的抑制不会影响PTTG1，这表明PTTG1调节c-myc的表达。此外，PTTG1表达水平与HCC患者生存率呈负相关，表明HCC患者具有独立的预后生物标志物。我们的数据表明PTTG1通过c-myc诱导参与TNF-α相关的HCC，并且PTTG1可能是HCC的潜在治疗靶标。

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PTTG1 is involved in TNF-α-related hepatocellular carcinoma via the induction of c-myc.

Hepatocellular carcinoma (HCC) is a malignant disease caused by a variety of factors. However, the genomic and molecular aberrations in HCC are largely unknown. Herein, pituitary tumor transforming gene 1 (PTTG1) was discovered as a potential inflammation-related oncogene in HCC, and its functions and molecular mechanisms were investigated. mRNA expression microarray, real-time polymerase chain reaction (PCR), immunohistochemistry, and western blotting analyses revealed that PTTG1 is upregulated in HCC. Further in vitro and in vivo studies indicated that the proinflammatory cytokine tumor necrosis factor-α (TNF-α) induces PTTG1 expression, and PTTG1 was found to upregulate c-myc, a well-known oncogene. Downregulation of PTTG1 reduced c-myc and proliferating cell nuclear antigen (PCNA) expression and inhibited cell proliferation. Interestingly, inhibition of c-myc by 10058-F4 did not affect PTTG1, which suggests that PTTG1 regulates c-myc expression. Furthermore, PTTG1 expression levels are inversely correlated with HCC patient survival, indicating an independent prognostic biomarker for patients with HCC. Our data demonstrate that PTTG1 is involved in TNF-α-related HCC via c-myc induction and that PTTG1 may be a potential therapeutic target for HCC.

更新日期：2019-08-06

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