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首页> 外文期刊>Cytokine >ROR-alpha-1 inhibits the proliferation, invasion, and migration of hepatocellular carcinoma MHCC97H via downregulation of chemokine CXCL5
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ROR-alpha-1 inhibits the proliferation, invasion, and migration of hepatocellular carcinoma MHCC97H via downregulation of chemokine CXCL5

机译：ROR-alpha-1通过趋化因子CXCL5的下调抑制肝细胞癌MHCC97H的增殖，侵袭和迁移

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/ Hepatocarcinogenesis is a complicated process that is affected by a variety of microenvironmental factors, such as secretory chemokines and cell-extracellular matrix (ECM). Retinoic acid receptor-related orphan receptor (ROR)-alpha has been shown to attenuate tumor invasiveness by inducing suppressive cell microenvironment, and its low expression was associated with a worse prognosis in HCC patients. In the present study, we attempted to investigate the role and mechanism of the dominant transcript of ROR-alpha, ROR-alpha-1, in HCC development and progression. Among the four transcripts (ROR-alpha-1/-2/-3/-4), overexpression of ROR-alpha-1 dramatically suppressed the capacity of MHCC97H cells to proliferate, migrate and invade. We analyzed the differentially expressed genes in ROR-alpha-1-overexpressed and non-overexpressed MHCC97H cells, performed Gene Ontology (GO) enrichment analysis on these differentially-expressed genes, and found out that factors involved in the tumor microenvironment and ECM are related to the anti-tumor effects of ROR-alpha-1. Among these factors, chemokine CXCL5 was significantly downregulated by ROR-alpha-1 overexpression. Overexpression of ROR-alpha-1 remarkably inhibited the capacity of HCC cells to proliferate, migrate, invade, and downregulated the protein levels of beta-catenin, c-Myc, Cyclin D1, and N-cadherin, suggesting the tumor-suppressive role of ROR-alpha-1 in MHCC97H cells. Moreover, overexpression of CXCL5 dramatically attenuated the suppressive effects of cell proliferation, migration and invasion induced by ROR-alpha-1 overexpression in MHCC97H, suggesting that ROR-alpha-1 exerts its anti-tumor effects via downregulating CXCL5. In conclusion, we demonstrate the tumor-suppressive role of ROR-alpha-1 in MHCC97H cells and that ROR-alpha-1 might play a tumor-suppressive role via regulation of chemokine CXCL5.
机译：/肝癌是一种复杂的过程，其受各种微环境的影响，例如分泌趋化因子和细胞 - 细胞外基质（ECM）。预先证明了视黄酸受体相关的孤儿（ROR） - 通过诱导抑制细胞微环境来衰减肿瘤侵犯性，其低表达与HCC患者的更糟糕的预后有关。在本研究中，我们试图探讨ROR-alpha，ROR-alpha-1，HCC开发和进展中显性转录物的作用和机制。在四个转录物（ROR-α-1 / -2 / -3 / -3）中，ROR-α-1的过表达显着抑制了MHCC97H细胞的能力，以增殖，迁移和侵入。我们分析了ROR-α-1-过表达和非过表达的MHCC97H细胞中的差异表达基因，对这些差异表达基因进行了基因本体学（GO）富集分析，发现肿瘤微环境和ECM中涉及的因素是相关的ROR-α-1的抗肿瘤作用。在这些因素中，趋化因子CXCl5通过ROR-α-1过表达显着下调。 ROR-α-1的过度表达显着抑制HCC细胞增殖，迁移，侵入的能力，迁移，侵入和下调β-连环蛋白，C-MYC，Cyclin D1和N-Cadherin的蛋白质水平，表明肿瘤抑制作用MHCC97H细胞中的ROR-α-1。此外，CXCL5的过度表达显着抑制了MHCC97H中ROR-α-1过表达诱导的细胞增殖，迁移和侵袭的抑制作用，表明ROR-α-1通过下调CXCL5施加其抗肿瘤作用。总之，我们证明了ROR-α-1在MHCC97H细胞中的肿瘤抑制作用，并且ROR-α-1可以通过调节趋化因子CXCL5来发挥肿瘤抑制作用。

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