Department of Clinical Pharmacy, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, No.100 Haining Road, Shanghai 200080, PR China.
Acta Biochim Biophys Sin (Shanghai). 2020 Apr 20;52(4):411-420. doi: 10.1093/abbs/gmaa014.
Vasculogenic mimicry (VM), a newly defined pattern of tumor blood supply, has been identified in several malignant tumors, including hepatocellular carcinoma (HCC). Rho kinase (ROCK) plays an important role in various types of cancers. However, whether ROCK participates in transforming growth factor-β1 (TGF-β1)-induced VM formation is unclear. Here, we evaluated the role of ROCK in TGF-β1-induced VM formation in HCC. Our findings showed that the TGF-β1/ROCK signaling pathway is involved in VM formation by inducing the epithelial-mesenchymal transition. Furthermore, TGF-β1 and ROCK were found to play distinct roles in the cancer stem cell phenotype during VM formation. These results provide insights into potential antitumor therapies for inhibiting VM by targeting the TGF-β1/ROCK signaling pathway in HCC.
血管生成拟态（VM），一种新定义的肿瘤血液供应模式，已在包括肝细胞癌（HCC）在内的几种恶性肿瘤中被识别。Rho 激酶（ROCK）在各种类型的癌症中发挥着重要作用。然而，ROCK 是否参与转化生长因子-β1（TGF-β1）诱导的 VM 形成尚不清楚。在这里，我们评估了 ROCK 在 TGF-β1 诱导的 HCC 中 VM 形成中的作用。我们的研究结果表明，TGF-β1/ROCK 信号通路通过诱导上皮-间充质转化参与 VM 的形成。此外，发现 TGF-β1 和 ROCK 在 VM 形成过程中的肿瘤干细胞表型中发挥不同的作用。这些结果为通过靶向 HCC 中的 TGF-β1/ROCK 信号通路抑制 VM 提供了潜在的抗肿瘤治疗思路。
