The Expression and Functional Significance of Runx2 in Hepatocellular Carcinoma: Its Role in Vasculogenic Mimicry and Epithelial–Mesenchymal Transition

Cao, Zi; Sun, Baocun; Zhao, Xiulan; Zhang, Yanhui; Gu, Qing; Liang, Xiaohui; Dong, Xueyi; Zhao, Nan

doi:10.3390/ijms18030500

Cited by 45 publications

(41 citation statements)

References 37 publications

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“…EMT is regulated by many transcription factors, including the traditional factor ZEB1. The role of EMT in the development of VM has recently attracted attention (9,15,16). Liu et al (8) confirmed that ZEB1 can promote VM formation by inducing EMT in colorectal cancer.…”

Section: Vasculogenic Mimicry In Bladder Cancer and Its Association Wmentioning

confidence: 82%

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Vasculogenic mimicry in bladder cancer and its association with the aberrant expression of ZEB1

Mao

Wang

et al. 2018

Oncol Lett

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Abstract. The aim of the present study was to investigate the associations between vasculogenic mimicry (VM) and zinc finger E-box binding homeobox 1 (ZEB1) in bladder cancer. VM structure and ZEB1 expression were analyzed by cluster of differentiation 34/periodic acid Schiff (PAS) double staining and immunohistochemical staining in 135 specimens from patients with bladder cancer, and a further 12 specimens from normal bladder tissues. Three-dimensional (3-D) culture was used to detect VM formation in the bladder transitional cancer cell lines UM-UC-3 and J82, and the immortalized human bladder epithelium cell line SV-HUC-1 in vitro. ZEB1 expression in these cell lines was compared by reverse transcription-quantitative polymerase chain reaction and western blot assays. In addition, small interfering RNA was used to inhibit ZEB1 in UM-UC-3 and J82 cells, followed by 3-D culturing of treated cell lines. As a result, VM was observed in 31.1% of specimens from bladder cancer tissues, and cases with high ZEB1 expression accounted for 60.0% of patients with bladder cancer. In addition, ZEB1 expression was closely associated with VM (r=0.189; P<0.05), and also increased as the grade and stage of the tumor developed. In an in vitro assay, UM-UC-3 and J82 cells exhibited VM formation, however, SV-HUC-1 did not. Furthermore, VM-forming cancer cell lines UM-UC-3 and J82 exhibited higher ZEB1 expression. Notably, VM formation was inhibited following knockdown of ZEB1. In conclusion, ZEB1 may be associated with VM in bladder cancer and serve an important role in the process of VM formation. However, its detailed mechanism requires further study.

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Section: Vasculogenic Mimicry In Bladder Cancer and Its Association Wmentioning

confidence: 82%

“…Some regulatory factors, such as Twist, Runx2 and ZEB2, play important roles in VM formation by promoting EMT (6,16,17). As a crucial EMT-inducer, ZEB1 was increased in colorectal carcinoma samples and its expression concomitantly occurred with EMT features in vivo and in vitro.…”

Section: Discussionmentioning

confidence: 99%

Vasculogenic mimicry in bladder cancer and its association with the aberrant expression of ZEB1

Mao

Wang

et al. 2018

Oncol Lett

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“…66 In hepatocellular carcinoma (HCC), Runx2 could promote EMT and VM formation, and Galectin-3 might play a role in this process. 67 Another study investigated VM formation and the EMT phenomenon in two HCC cell lines, MHCC97-H and HepG2, with high and low Notch1 expression, respectively, and confirmed that Notch1 could promote HCC progression by activating the EMT pathway and VM formation. 68 In colon cancer cells, the downregulation of hypoxia-inducible factor 1-alpha (HIF-1α), which functions as a master transcriptional regulator of the adaptive response to hypoxia, could reduce VM and the expression of EMT markers, such as E-cadherin, claudin-4, Vim, and Fn1, in HCT-116 cells.…”

Section: Epithelial-mesenchymal Transition and Vasculogenic Mimicrymentioning

confidence: 87%

Traditional Chinese medicine as targeted treatment for epithelial‐mesenchymal transition‐induced cancer progression

Liu

Fei

Cheng

et al. 2018

J of Cellular Biochemistry

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The epithelial‐mesenchymal transition (EMT) program, which loosens cell‐cell adhesion complexes, endows cells with enhanced migratory and invasive properties. Furthermore, this process facilitates both the development of drug resistance and immunosuppression by tumor cells, which preclude the successful treatment of cancer. Recent research has demonstrated that many signaling pathways are involved in EMT progression. In addition, cancer stem cells (CSCs), vasculogenic mimicry (VM) and the tumor‐related immune microenvironment all play important roles in tumor formation. However, there are few reports on the relationships between EMT and these factors. In addition, in recent years, traditional Chinese medicine (TCM) has developed a unique system for treating cancer. In this review, we summarize the crucial signaling pathways associated with the EMT process in cancer patients and discuss the interconnections between EMT and other molecular factors (such as CSCs, VM, and the tumor‐related immune microenvironment). We attempt to identify common regulators that might be potential therapeutic targets to thereby optimize tumor treatment. In addition, we outline recent research on TCM approaches that target EMT and thereby provide a foundation for further research on the exact mechanisms by which TCMs affect EMT in cancer.

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“…2B). PAS/CD34 staining was used to better distinguish VM from general endothelium-dependent blood vessels [30-34]. ST2 expression (Fig.…”

Section: Resultsmentioning

confidence: 99%

IL-33/ST2 Axis Regulates Vasculogenic Mimicry via ERK1/2-MMP-2/9 Pathway in Melanoma

et al. 2019

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Background: Melanoma, an extremely malignant form of cancer, poses a significant health risk. Vasculogenic mimicry (VM), blood vessels formed by tumor cells instead of endothelial cells, is an important factor for the rapid progression of melanoma. Interleukin (IL)-33 is an inflammatory factor commonly found in the tumor microenvironment and plays an important role in the progression of many tumors. IL-33 acts on immune cells and tumor cells through its receptor ST2. This study hypothesized that IL-33 directly affects the progression of melanoma. Objectives: This study was designed to investigate the effect of IL-33 on VM of melanoma and its potential mechanism of action. Methods: The expression of ST2 was evaluated in 66 cases of melanoma collected from human patients, and the differences were analyzed. In vitro experiments were conducted to study the effects of the IL-33/ST2 axis on cell migration and invasion and to elucidate possible mechanisms. Results: ST2 expression is associated with that of matrix metalloproteinase (MMP)-2 and VM in melanoma of patients. IL-33 increases the abilities of proliferation, migration and invasion of melanoma cells and VM tube formation through ST2. IL-33 induces the production of MMP-2/9 via ERK1/2 phosphorylation. Conclusion: IL-33 can directly act on melanoma cells and promote its development.

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The Expression and Functional Significance of Runx2 in Hepatocellular Carcinoma: Its Role in Vasculogenic Mimicry and Epithelial–Mesenchymal Transition

Cited by 45 publications

References 37 publications

Vasculogenic mimicry in bladder cancer and its association with the aberrant expression of ZEB1

Vasculogenic mimicry in bladder cancer and its association with the aberrant expression of ZEB1

Traditional Chinese medicine as targeted treatment for epithelial‐mesenchymal transition‐induced cancer progression

IL-33/ST2 Axis Regulates Vasculogenic Mimicry via ERK1/2-MMP-2/9 Pathway in Melanoma

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