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首页> 外文期刊>Cellular Physiology and Biochemistry >PRMT1 Promoted HCC Growth and Metastasis In Vitro and In Vivo via Activating the STAT3 Signalling Pathway
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PRMT1 Promoted HCC Growth and Metastasis In Vitro and In Vivo via Activating the STAT3 Signalling Pathway

机译：PRMT1通过激活STAT3信号通路促进了HCC的体外生长和转移。

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Background/Aims Although it has been widely accepted that protein arginine methyltransferase 1 (PRMT1) is a cancer-promoting gene in various cancers, the mechanism of PRMT1 in hepatocellular carcinoma (HCC) requires more exploration. This study aimed to investigate the role of PRMT1 in HCC growth and metastasis. Methods We compared PRMT1 expression and clinicopathological characteristics using paired HCC and adjacent noncancerous liver tissues from 210 patients and immunohistochemistry analyses. Cell proliferation, colony formation and migration were determined in HCC cell lines with PRMT1 overexpression or downregulation through MTT, crystal violet and Boyden chamber assays. Tumour growth was monitored in a xenograft model, and intrahepatic metastasis models were established. Results PRMT1 expression was greatly increased in clinical HCC samples and strongly associated with poor prognosis and recurrence; PRMT1 expression was also positively correlated with microvascular invasion (P = 0.024), tumour differentiation (P = 0.014), tumour size (P = 0.002), and portal vein tumour thrombus (PVTT) (P = 0.028). Cell proliferation, colony formation and migration in vitro were enhanced by PRMT1 upregulation and decreased by PRMT1 downregulation in HCC cell lines. Moreover, low PRMT1 expression resulted in slow tumour growth and decreased tumour weight in vivo, as well as tumour metastasis. These phenotypes were associated with STAT3 signalling pathway activation. Cryptotanshinone, a STAT3 inhibitor, inhibited STAT3 phosphorylation and reversed the HCC phenotype of PRMT1 expression. Conclusions We revealed a significant role for PRMT1 in HCC progression and metastasis in vitro and in vivo via STAT3 signalling pathway activation. PRMT1 may be a potential novel prognostic biomarker and new therapeutic target for HCC.
机译：背景/目的尽管精氨酸甲基转移酶1（PRMT1）是各种癌症中的促癌基因已广为接受，但PRMT1在肝细胞癌（HCC）中的机制尚需进一步探索。这项研究旨在调查PRMT1在肝癌生长和转移中的作用。方法我们采用配对的HCC和210例患者的非癌性肝组织进行了PRMT1的表达和临床病理特征的比较，并进行了免疫组织化学分析。通过MTT，结晶紫和Boyden室测定法，在PRMT1过表达或下调的HCC细胞系中确定细胞增殖，集落形成和迁移。在异种移植模型中监测肿瘤的生长，并建立肝内转移模型。结果PRMT1表达在临床HCC样本中大大增加，并与不良预后和复发密切相关。 PRMT1表达也与微血管浸润（P = 0.024），肿瘤分化（P = 0.014），肿瘤大小（P = 0.002）和门静脉肿瘤血栓（PVTT）（P = 0.028）呈正相关。在肝癌细胞系中，PRMT1的上调增强了体外细胞的增殖，集落形成和迁移，而PRMT1的下调则降低了体外增殖。此外，低PRMT1表达导致体内肿瘤生长缓慢，体内肿瘤重量减少以及肿瘤转移。这些表型与STAT3信号通路激活相关。 STAT3抑制剂隐丹参酮抑制STAT3磷酸化并逆转PRMT1表达的HCC表型。结论我们通过STAT3信号通路激活揭示了PRMT1在体内外HCC进展和转移中的重要作用。 PRMT1可能是潜在的新型预后生物标志物和肝癌的新治疗靶标。

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