Abstract
Vasculogenic mimicry refers to the process by which highly invasive cancer cells mimic endothelial cells by forming blood channels. Vasculogenic mimicry is important for the invasion and metastasis of tumor cells in colorectal cancer. STAT3 was initially identified as a mediator of the inflammation-associated acute phase response. The phosphorylation of Signal Transducers and Activators of Transcription 3 (p-STAT3) is closely related to tumor invasion and migration. We analyzed the relationship between p-STAT3 and vasculogenic mimicry formation in 65 human colorectal cancer samples, and the results showed that the expression of p-STAT3 is significantly correlated with vasculogenic mimicry, tumor metastasis, Tumor, Lymph Node and Metastasis Stage (TNM Stage), and poor prognosis. It is known that interleukin 6 can induce the phosphorylation of STAT3. We found that using interleukin 6 to induce p-STAT3 activation in colorectal cancer cell lines can result in vasculogenic mimicry and using AG490 to suppress p-STAT3 activation restrained vasculogenic mimicry. Furthermore, the state of p-STAT3 activation can affect epithelial-to-mesenchymal transition. By immunofluorescence double staining, we discovered that p-STAT3 expression is more directly correlated with the epithelial-to-mesenchymal transition marker vimentin than with the vasculogenic mimicry-related protein VE-cadherin. These data show that activated p-STAT3 upregulates epithelial-to-mesenchymal transition–related proteins and promotes vasculogenic mimicry.
Highlights
Colorectal cancer (CRC) is the third most frequently diagnosed cancer worldwide, and most patients are diagnosed with advanced disease.[1]
It has been demonstrated that p-Signal Transducers and Activators of Transcription 3 (STAT3) activation is required to sustain epithelial-to-mesenchymal transition (EMT)-associated phenotypes in ovarian and breast cancers.[20,21]
Our results support the potential role of p-STAT3 activation in promoting metastasis and EMT and inducing the formation of vasculogenic mimicry (VM) patterns in CRC
Summary
Colorectal cancer (CRC) is the third most frequently diagnosed cancer worldwide, and most patients are diagnosed with advanced disease.[1] the accepted principle underlying tumor survival and metastatic potentials has been the tumor microenvironment and vascular network formation.[2] It is known that endothelial cells can form blood vessels. Angiogenesis is not the only process by which tumors acquire their blood supply. Malignant tumor cells can line up to form functional blood vessels in a mechanism called vasculogenic mimicry (VM).[2,3]. Vasculogenic mimicry refers to the process by which highly invasive cancer cells mimic endothelial cells by forming blood
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