Mig-7 expression and vasculogenic mimicry in malignant ovarian tumors

Czekierdowski, Artur; Czekierdowska, Sylwia; Stachowicz, Norbert; Łoziński, Tomasz; Gurynowicz, Grzegorz

doi:10.5603/gp.a2017.0100

Cited by 6 publications

(5 citation statements)

References 29 publications

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“…Interestingly, high expression of VE-cadherin and EphA2 has been found in clinical samples from ovarian cancer patients that exhibit a highly invasive phenotype (84, 85). Additionally, other studies demonstrated that MMP-2 and MMP-14 are also overexpressed in ovarian cancer samples, which is associated with poor clinical outcome (38, 86).…”

Section: Mechanisms and Signaling Molecules Involved In Vm In Ovarianmentioning

confidence: 99%

“…Furthermore, Ln5γ2 activates the endothelial growth factor receptor (EGFR) which promotes the expression of the migration-inducing protein 7 (Mig-7), stimulating invasion and VM (94). A study carried out in ovarian cancer samples revealed an association of VM with VE-cadherin and Mig-7 expression (84). It was observed that ovarian tumors without VM frequently expressed low levels of VE-cadherin compared to those with VM.…”

Section: Mechanisms and Signaling Molecules Involved In Vm In Ovarianmentioning

confidence: 99%

“…It was observed that ovarian tumors without VM frequently expressed low levels of VE-cadherin compared to those with VM. Meanwhile, Mig-7 expression was increased in tumor samples compared to normal tissues, positively correlating with VM and VE-cadherin expression (84).…”

Section: Mechanisms and Signaling Molecules Involved In Vm In Ovarianmentioning

confidence: 99%

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Mechanisms of Vasculogenic Mimicry in Ovarian Cancer

et al. 2019

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Solid tumors carry out the formation of new vessels providing blood supply for growth, tumor maintenance, and metastasis. Several processes take place during tumor vascularization. In angiogenesis, new vessels are derived from endothelial cells of pre-existing vessels; while in vasculogenesis, new vessels are formed de novo from endothelial progenitor cells, creating an abnormal, immature, and disorganized vascular network. Moreover, highly aggressive tumor cells form structures similar to vessels, providing a pathway for perfusion; this process is named vasculogenic mimicry (VM), where vessel-like channels mimic the function of vessels and transport plasma and blood cells. VM is developed by numerous types of aggressive tumors, including ovarian carcinoma which is the second most common cause of death among gynecological cancers. VM has been associated with poor patient outcome and survival in ovarian cancer, although the involved mechanisms are still under investigation. Several signaling molecules have an important role in VM in ovarian cancer, by regulating the expression of genes related to vascular, embryogenic, and hypoxic signaling pathways. In this review, we provide an overview of the current knowledge of the signaling molecules involved in the promotion and regulation of VM in ovarian cancer. The clinical implications and the potential benefit of identification and targeting of VM related molecules for ovarian cancer treatment are also discussed.

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Section: Mechanisms and Signaling Molecules Involved In Vm In Ovarianmentioning

confidence: 99%

Section: Mechanisms and Signaling Molecules Involved In Vm In Ovarianmentioning

confidence: 99%

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Mechanisms of Vasculogenic Mimicry in Ovarian Cancer

et al. 2019

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“…VE-cadherin expression was highly upregulated in VM-positive patients and in SKOV3 and OVCAR3 ovarian cancer cells under hypoxic conditions (45). It has also been shown that VE-cadherin expression levels are closely associated with the propensity for VM in ovarian cancer cells and malignant ovarian cancer tissues (46,47), suggesting biological significance of VE-cadherin in VM in malignant ovarian cancers.…”

Section: Vascular/angiogenesis Signaling In Vmmentioning

confidence: 95%

Angiogenesis and vasculogenic mimicry as therapeutic targets in ovarian cancer

Lim

Kwon

et al. 2020

BMB Rep.

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Tumor angiogenesis is an essential process for growth and metastasis of cancer cells as it supplies tumors with oxygen and nutrients. During tumor angiogenesis, many pro-angiogenic factors are secreted by tumor cells to induce their own vascularization via activation of pre-existing host endothelium. However, accumulating evidence suggests that vasculogenic mimicry (VM) is a key alternative mechanism for tumor vascularization when tumors are faced with insufficient supply of oxygen and nutrients. VM is a tumor vascularization mechanism in which tumors create a blood supply system, in contrast to tumor angiogenesis mechanisms that depend on pre-existing host endothelium. VM is closely associated with tumor progression and poor prognosis in many cancers. Therefore, inhibition of VM may be a promising therapeutic strategy and may overcome the limitations of anti-angiogenesis therapy for cancer patients. In this review, we provide an overview of the current anti-angiogenic therapies for ovarian cancer and the current state of knowledge regarding the links between microRNAs and the VM process, with a focus on the mechanism that regulates associated signaling pathways in ovarian cancer. Moreover, we discuss the potential for VM as a therapeutic strategy against ovarian cancer. [

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“…Mig-7 significantly affects tumor migration and invasion in hepatocellular carcinoma and osteosarcoma, while it is essential for proliferation and invasion in ovarian cancer [8,9]. Further, Mig-7 is overexpressed in highly invasive tumors but not in non-invasive malignant cells [10][11][12][13], suggesting an important role in tumor invasion. Additionally, knocking down Mig-7 attenuates the invasiveness of U87MG cells [12].…”

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confidence: 98%

Migration-inducing gene-7 promotes glioma cell proliferation and invasiveness via activating the MAPK signaling pathway

Pan,

Chen,

Huang

et al. 2023

neo

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Glioma is a highly aggressive primary malignant tumor. Migration-inducing gene-7 (Mig-7) is closely related to tumor invasion and metastasis. However, the detailed molecular mechanism of Mig-7-mediated promotion of glioma cell invasion requires further investigation. Therefore, this study aimed to investigate the molecular mechanism by which Mig-7 promotes invasion and growth of glioma tumor cells. After collecting 65 glioma tissues and 16 non-tumor tissues, the expression difference of Mig-7 between tumor tissues and non-tumor tissues was analyzed. The molecular mechanism of Mig-7 in tumor cells was investigated by knockdown or overexpression of Mig-7 in U87MG cells. Specifically, the expression levels of mitogen-activated protein kinase (MAPK) signaling pathway-related molecules were detected in cells that knocked down Mig-7. MTT, Transwell, and three-dimensional cell culture assays were used to detect the survival, migration, invasion, and tube formation of U87MG cells that overexpressed Mig-7 were treated with the MAPK signaling pathway inhibitors (SP600125, SCH772984, and SB202190). The effect of Mig-7 on the tumorigenic ability of U87MG cells was investigated by subcutaneous tumorigenic experiment in nude mice. The corresponding results indicated that Mig-7 expression was significantly higher in glioma tissues and cell lines compared to that in non-neoplastic brain tissues and normal glial cell lines. In U87MG cells, downregulation or overexpression of Mig-7 inhibited or promoted the expression of MMP-2, MMP-9, LAMC2, EphA2, and VE-cadherin, and phosphorylation levels of ERK1/2, JNK, and p38. Mig-7 overexpression promoted migration, invasion, cell viability, and tube formation, which were reversed by the MAPK signaling pathway inhibitors. Mig-7 overexpression promoted subcutaneous tumor growth in mice and upregulated the phosphorylation levels of ERK1/2, JNK, and p38 and the expression of Ki-67. These effects of Mig-7 overexpression were reversed by MAPK pathway inhibitors. Overall, these results suggest that Mig-7 may be a novel biomarker and potential therapeutic target for glioma, with the MAPK pathway playing a key role in the corresponding Mig-7 mechanism of action.

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Mig-7 expression and vasculogenic mimicry in malignant ovarian tumors

Cited by 6 publications

References 29 publications

Mechanisms of Vasculogenic Mimicry in Ovarian Cancer

Mechanisms of Vasculogenic Mimicry in Ovarian Cancer

Angiogenesis and vasculogenic mimicry as therapeutic targets in ovarian cancer

Migration-inducing gene-7 promotes glioma cell proliferation and invasiveness via activating the MAPK signaling pathway

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