Cyr61 from adipose‐derived stem cells promotes colorectal cancer metastasis and vasculogenic mimicry formation via integrin αVβ5

Liang, Zhenxing; Liu, Huashan; Zhang, Yunfeng; Xiong, Li; Zeng, Ziwei; He, Xiaowen; Wang, Fengwei; Wu, Xianrui; Lan, Ping

doi:10.1002/1878-0261.12998

Cited by 19 publications

(9 citation statements)

References 63 publications

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“…In addition, Habel et al [56] found that knockdown of CYR61 expression in osteosarcoma downregulates various angiogenic proteins, including VEGF-A, leading to suppression of tumor angiogenesis. More recently, signal transducer and activator of transcription 3 (STAT3), a member of the STAT family that plays an important role in cell proliferation, differentiation, apoptosis, tumorigenesis, and angiogenesis [57], was detected in exosomes secreted from colorectal cancer cells; these exosomes have been shown to induce adipose-derived stem cells to upregulate CYR61 expression, yielding the formation by colorectal cancer cells of vasculature-mimicking tissue via a VEGF-independent process [58].…”

Section: The Possible Existence Of Vegf-independent and Vegfr2-depend...mentioning

confidence: 99%

VEGF-Independent Angiogenic Factors: Beyond VEGF/VEGFR2 Signaling

2022

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Tumors induce angiogenesis to acquire oxygen and nutrition from their adjacent microenvironment. Tumor angiogenesis has been believed to be induced primarily by the secretion of vascular endothelial growth factor-A (VEGF-A) from various tumors. VEGF-A binds to VEGF receptor 2 (VEGFR2), resulting in subsequent activation of cellular substances regulating cell proliferation, survival, and angiogenesis. Antiangiogenic therapies targeting the VEGF-A/VEGFR2 axis, including bevacizumab and ramucirumab, humanized monoclonal antibodies against VEGF-A and VEGFR2, respectively, have been proposed as a promising strategy aimed at preventing tumor growth, invasion, and metastasis. Phase III clinical trials using bevacizumab and ramucirumab have shown that not all tumor patients benefit from such antiangiogenic agents, and that some patients who initially benefit subsequently become less responsive to these antibodies, suggesting the possible existence of VEGF-independent angiogenic factors. In this review, we focus on VEGF-independent and VEGFR2-dependent tumor angiogenesis, as well as VEGFR2-independent tumor angiogenesis. Additionally, we discuss VEGF-independent angiogenic factors which have been reported in previous studies. Various molecular targeting drugs are currently being evaluated as potential antitumor therapies. We expect that precision medicine will permit the development of innovative antiangiogenic therapies targeting individual angiogenic factors selected on the basis of the genetic screening of tumors.

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Section: The Possible Existence Of Vegf-independent and Vegfr2-depend...mentioning

confidence: 99%

VEGF-Independent Angiogenic Factors: Beyond VEGF/VEGFR2 Signaling

2022

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“…This results in an increased cell migration and invasion, as well as CRC metastasis. Inhibition of the STAT3 signaling could decrease the expression of Snail1, Twist1, and MMP2 (40,41). Here, TRIM6 knockdown decreased the expression of Snail1, Twist1, and MMP2 (Figure 1), which may be due to the decreased phosphorylation of STAT3 through inhibiting the ubiquitination of SOCS2.…”

Section: Discussionmentioning

confidence: 89%

Tripartite Motif Protein 6 Promotes Colorectal Cancer Cell Migration and Metastasis via SOCS2-STAT3 Signaling

et al. 2021

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Colorectal cancer (CRC) is one of the leading causes of cancer death worldwide, with most mortalities being caused by metastases. However, the underlying molecular mechanism of CRC metastases remains largely unknown. Emerging evidence has shown the role of the tripartite motif family, especially tripartite motif protein 6 (TRIM6), in carcinogenesis. In this study, we used CRC cell lines with TRIM6 knockdown and overexpression to investigate the function of TRIM6 in CRC metastasis. We found that TRIM6 promotes CRC cell migration and invasion both in vitro and in vivo. TRIM6 knockdown slows down the migration and invasion processes, whereas TRIM6 overexpression accelerates CRC cell migration and invasion. TRIM6 is potentially the upstream regulatory factor for signal transducer and activator of transcription 3 (STAT3) via the suppressor of cytokine signaling 2 (SOCS2). A total of 70 samples from patients with CRC further confirmed that TRIM6 expression level is positively correlated with STAT3 phosphorylation and negatively correlated with SOCS2 expression. Therefore, TRIM6 could be a potential therapeutic target for CRC metastasis.

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“…28 Malignant tumor cells can form tubular neovascularization by VM to promote cancer invasion. 29,30 Epithelial-mesenchymal transition seems to be connected with the VM process of tumor migration in prior research. 31 Emerging studies have unveiled that F. nucleatum affected METTL3 to modulate CRC occurrence and aggressiveness.…”

Section: Introductionmentioning

confidence: 93%

“…Methyltransferase‐like 3 could promote tumor cell invasion and migration by accelerating EMT formation 28 . Malignant tumor cells can form tubular neovascularization by VM to promote cancer invasion 29,30 . Epithelial–mesenchymal transition seems to be connected with the VM process of tumor migration in prior research 31 .…”

Section: Introductionmentioning

confidence: 99%

Clostridium butyricum inhibits epithelial–mesenchymal transition of intestinal carcinogenesis through downregulating METTL3

Zhang

Dong

et al. 2023

Cancer Science

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Colorectal cancer (CRC) is related to gut microbiota dysbiosis, especially butyrateproducing bacteria reduction. Our previous study suggested that administration of Clostridium butyricum, a butyrate-producing bacterium, exerts a crucial effect against CRC, however the potential mechanism is not clear. We first found that methyltransferase-like 3 (METTL3) showed a positive correlation with proliferation, epithelial-mesenchymal transition (EMT), DNA repair, metastasis, and invasion in a database analysis. The expression of METTL3 gradually increased from human normal colon tissue, to adenoma, and carcinoma, and was positively correlated with Ecadherin and CD34 levels. Overexpression of METTL3 promoted the proliferation, migration, and invasion of CRC cells and induced vasculogenic mimicry (VM) formation. Clostridium butyricum could downregulate METTL3 expression in CRC cells and decrease the expression of vimentin and vascular endothelial growth factor receptor 2 to reduce EMT and VM formation. Clostridium butyricum alleviated the pro-oncogenic effect of METTL3 overexpressing plasmid in CRC cells. The anti-EMT effect on METTL3 reduction of C. butyricum could be blunted by knocking down Gprotein coupled receptor 43. Moreover, C. butyricum prevented EMT and VM and inhibited tumor metastasis in nude mice. Accordingly, C. butyricum could inhibit EMT and VM formation of intestinal carcinogenesis through downregulating METTL3.These findings broaden our understanding of probiotics supplement in CRC prevention and treatment.

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Cyr61 from adipose‐derived stem cells promotes colorectal cancer metastasis and vasculogenic mimicry formation via integrin α_Vβ₅

Abstract: Cyr61 from adipose-derived stem cells promotes colorectal cancer metastasis and vasculogenic mimicry formation via integrin α V β 5

Cited by 19 publications

References 63 publications

VEGF-Independent Angiogenic Factors: Beyond VEGF/VEGFR2 Signaling

VEGF-Independent Angiogenic Factors: Beyond VEGF/VEGFR2 Signaling

Tripartite Motif Protein 6 Promotes Colorectal Cancer Cell Migration and Metastasis via SOCS2-STAT3 Signaling

Clostridium butyricum inhibits epithelial–mesenchymal transition of intestinal carcinogenesis through downregulating METTL3

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