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  • 1
    Online Resource
    Online Resource
    Significance of Vasculogenic Mimicry Formation in Gastric Carcinoma
    S. Karger AG ; 2017
    In:  Oncology Research and Treatment Vol. 40, No. 1-2 ( 2017), p. 35-41
    Details
    In: Oncology Research and Treatment, S. Karger AG, Vol. 40, No. 1-2 ( 2017), p. 35-41
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 The purpose of this study was to evaluate the clinical significance and prognostic roles of vasculogenic mimicry (VM) and elucidate their intrinsic association with molecular markers. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 89 human gastric cancer cases with detailed follow-up and clinicopathologic data were collected. CD34/periodic acid-Schiff double staining was performed to validate the existence of VM. Immunohistochemistry was performed to explore the expression of different molecular factors. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 VM was observed in 24 gastric cancer patients. They were prone to higher histological grade, hematogenous metastasis, distant recurrence, and chance of progression to stage III or IV (p 〈 0.05). The VM group had shorter overall and disease-free survival (p 〈 0.05). VM negativity was independently prognostic for prolonged overall or disease-free survival (p 〈 0.05). VM was positively associated with levels of matrix metalloproteinase-2, matrix metalloproteinase-9, vascular endothelial growth factor, and vascular endothelial growth factor receptor-1 (p 〈 0.05), but not with vascular endothelial growth factor receptor-2 (p 〉 0.05). 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 VM should be regarded as a good marker to indicate pathobiological behaviors of gastric cancer. Using antibodies against matrix metalloproteinases, vascular endothelial growth factor, or vascular endothelial growth factor receptors could be strategies to counteract VM formation.
    Type of Medium: Online Resource
    ISSN: 2296-5270 , 2296-5262
    URL: Article
    DOI: 10.1159/000455144
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2017
    detail.hit.zdb_id: 2749752-5
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  • 2
    Online Resource
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    HMGA2 promotes vasculogenic mimicry and tumor aggressiveness by upregulating Twist1 in gastric carcinoma
    Springer Science and Business Media LLC ; 2017
    In:  Scientific Reports Vol. 7, No. 1 ( 2017-05-22)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 7, No. 1 ( 2017-05-22)
    Abstract: High mobility group protein A2 (HMGA2) is a transcription factor that plays an important role in the invasion and metastasis of gastric carcinoma (GC). The term vasculogenic mimicry (VM) refers to the unique ability of aggressive tumour cells to mimic the pattern of embryonic vasculogenic networks. However, the relationship between HMGA2 and VM formation remains unclear. In the present study, we examined concomitant HMGA2 expression and VM in 228 human GC samples and 4 GC cell lines. Our data indicate that HMGA2 is not only significantly associated with VM formation but also influences the prognosis of patients with gastric carcinoma. Overexpression of HMGA2 significantly increased cell motility, invasiveness, and VM formation both in vitro and in vivo . A luciferase reporter assay, Co-IP and ChIP demonstrated that HMGA2 induced the expression of Twist1 and VE-cadherin by binding to the Twist1 promoter. Moreover, we observed a decrease in VE-cadherin following Twist1 knockdown in cells overexpressing HMGA2. This study indicates that HMGA2 promotes VM in GC via Twist1-VE-cadherin signalling and influences the prognosis of patients with GC.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/s41598-017-02494-6
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2017
    detail.hit.zdb_id: 2615211-3
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  • 3
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    Slug promoted vasculogenic mimicry in hepatocellular carcinoma
    Wiley ; 2013
    In:  Journal of Cellular and Molecular Medicine Vol. 17, No. 8 ( 2013-08), p. 1038-1047
    Details
    In: Journal of Cellular and Molecular Medicine, Wiley, Vol. 17, No. 8 ( 2013-08), p. 1038-1047
    Abstract: Vasculogenic mimicry ( VM ) refers to the unique capability of aggressive tumour cells to mimic the pattern of embryonic vasculogenic networks. Epithelial–mesenchymal transition ( EMT ) regulator slug have been implicated in the tumour invasion and metastasis of human hepatocellular carcinoma ( HCC ). However, the relationship between slug and VM formation is not clear. In the study, we demonstrated that slug expression was associated with EMT and cancer stem cell (CSCs) phenotype in HCC patients. Importantly, slug showed statistically correlation with VM formation. We consistently demonstrated that an overexpression of slug in HCC cells significantly increased CSC s subpopulation that was obvious by the increased clone forming efficiency in soft agar and by flowcytometry analysis. Meantime, the VM formation and VM mediator overexpression were also induced by slug induction. Finally, slug overexpression lead to the maintenance of CSC s phenotype and VM formation was demonstrated in vivo . Therefore, the results of this study indicate that slug induced the increase and maintenance of CSC s subpopulation and contributed to VM formation eventually. The related molecular pathways may be used as novel therapeutic targets for the inhibition of HCC angiogenesis and metastasis.
    Type of Medium: Online Resource
    ISSN: 1582-1838 , 1582-4934
    URL: Issue
    URL: Article
    DOI: 10.1111/jcmm.2013.17.issue-8
    DOI: 10.1111/jcmm.12087
    Language: English
    Publisher: Wiley
    Publication Date: 2013
    detail.hit.zdb_id: 2076114-4
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  • 4
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    Rictor regulates the vasculogenic mimicry of melanoma via the AKT ‐ MMP ‐2/9 pathway
    Wiley ; 2017
    In:  Journal of Cellular and Molecular Medicine Vol. 21, No. 12 ( 2017-12), p. 3579-3591
    Details
    In: Journal of Cellular and Molecular Medicine, Wiley, Vol. 21, No. 12 ( 2017-12), p. 3579-3591
    Abstract: Vasculogenic mimicry ( VM )‐positive melanomas are usually associated with poor prognosis. Rictor, the key component of the rapamycin‐insensitive complex of mTOR ( mTORC 2), is up‐regulated in several cancers, especially in melanomas with poor prognosis. The aim of this study was to investigate the role of Rictor in the regulation of VM and the mechanism underlying this possible regulation. VM channels were found in 35 of 81 tested melanoma samples and high Rictor expression correlated with VM structures. Moreover, Kaplan–Meier survival curves indicated that VM structures and high Rictor expression correlated with shorter survival in patients with melanoma. In vitro , Rictor knockdown by short hairpin RNA (sh RNA ) significantly inhibited the ability of A375 and MUM ‐2B melanoma cells to form VM structures, as evidenced by most tubes remaining open. Cell cycle analysis revealed that Rictor knockdown blocked cell growth and resulted in the accumulation of cells in G2/M phase, and cell migration and invasion were greatly affected after Rictor down‐regulation. Western blotting assays indicated that down‐regulating Rictor significantly inhibited the phosphorylation of AKT at Ser 473 and Thr 308 , which subsequently inhibited the expression and activity of downstream MMP ‐2/9, as confirmed by real‐time PCR and gelatin Zymography. MK ‐2206, a small‐molecule inhibitor of AKT , similarly inhibited the activity of AKT and secretion of MMP ‐2/9, further supporting that Rictor down‐regulation inhibits the phosphorylation of AKT and activity of downstream MMP ‐2/9 to affect VM formation. In conclusion, Rictor plays an important role in melanoma VM via the Rictor— AKT — MMP ‐2/9 signalling pathway.
    Type of Medium: Online Resource
    ISSN: 1582-1838 , 1582-4934
    URL: Issue
    URL: Article
    DOI: 10.1111/jcmm.2017.21.issue-12
    DOI: 10.1111/jcmm.13268
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 2076114-4
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  • 5
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    Hypoxia promotes vasculogenic mimicry formation by inducing epithelial–mesenchymal transition in ovarian carcinoma
    Elsevier BV ; 2014
    In:  Gynecologic Oncology Vol. 133, No. 3 ( 2014-06), p. 575-583
    Details
    In: Gynecologic Oncology, Elsevier BV, Vol. 133, No. 3 ( 2014-06), p. 575-583
    Type of Medium: Online Resource
    ISSN: 0090-8258
    URL: Article
    DOI: 10.1016/j.ygyno.2014.02.034
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2014
    detail.hit.zdb_id: 1467974-7
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  • 6
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    High expression of eIF4E is associated with tumor macrophage infiltration and leads to poor prognosis in breast cancer
    Springer Science and Business Media LLC ; 2021
    In:  BMC Cancer Vol. 21, No. 1 ( 2021-12)
    Details
    In: BMC Cancer, Springer Science and Business Media LLC, Vol. 21, No. 1 ( 2021-12)
    Abstract: The expression and activation of eukaryotic translation initiation factor 4E (eIF4E) is associated with cell transformation and tumor initiation, but the functional role and the mechanism whereby it drives immune cell infiltration in breast cancer (BRCA) remain uncertain. Methods Oncomine, Timer and UALCAN were used to analyze the expression of eIF4E in various cancers. PrognoScan, Kaplan–Meier plotter, and GEPIA were utilized to analyze the prognostic value of eIF4E in select cancers. In vitro cell experiments were used to verify the role of eIF4E in promoting the progression of BRCA. ImmuCellAI and TIMER database were used to explore the relationship between eIF4E and tumor infiltrating immune cells. The expression of a macrophage marker (CD68 + ) and an M2-type marker (CD163 + ) was evaluated using immunohistochemistry in 50 invasive BRCA samples on tissue microarrays. The Human Protein Atlas (HPA) database was used to show the expression of eIF4E and related immune markers. LinkedOmics and NetworkAnalyst were used to build the signaling network. Results Through multiple dataset mining, we found that the expression of eIF4E in BRCA was higher than that in normal tissues, and patients with increased eIF4E expression had poorer survival and a higher cumulative recurrence rate in BRCA. At the cellular level, BRCA cell migration and invasion were significantly inhibited after eIF4E expression was inhibited by siRNA. Immune infiltration analysis showed that the eIF4E expression level was significantly associated with the tumor purity and immune infiltration levels of different immune cells in BRCA. The results from immunohistochemical (IHC) staining further proved that the expression of CD68 + and CD163 + were significantly increased and correlated with poor prognosis in BRCA patients ( P   〈  0.05). Finally, interaction network and functional enrichment analysis revealed that eIF4E was mainly involved in tumor-related pathways, including the cell adhesion molecule pathway and the JAK-STAT signaling pathway. Conclusions Our study has demonstrated that eIF4E expression has prognostic value for BRCA patients. eIF4E may act as an essential regulator of tumor macrophage infiltration and may participate in macrophage M2 polarization.
    Type of Medium: Online Resource
    ISSN: 1471-2407
    URL: Article
    DOI: 10.1186/s12885-021-09010-0
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2021
    detail.hit.zdb_id: 2041352-X
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  • 7
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    S1PR1 regulates the switch of two angiogenic modes by VE-cadherin phosphorylation in breast cancer
    Springer Science and Business Media LLC ; 2019
    In:  Cell Death & Disease Vol. 10, No. 3 ( 2019-02-27)
    Details
    In: Cell Death & Disease, Springer Science and Business Media LLC, Vol. 10, No. 3 ( 2019-02-27)
    Abstract: Angiogenesis in solid tumors is divided into two modes: endothelium-dependent vessel (EDV) and vasculogenic mimicry (VM). Sphingosine-1-phosphate receptor 1 (S1PR1) plays a vital role on EDV in a variety of human tumors. However, the relationship between S1PR1 and VM is not clear. The aim of this study is to investigate S1PR1 on the regulation of EDV and mimicry formation in breast cancer. Here we show that S1PR1 phosphorylates the complex of VE-cadherin to regulate the switch of EDV and mimicry formation. Suppression of S1PR1 impairs EDV, but contributes to the generation of VM, invasion, and metastasis in vivo and vitro. By inhibiting RhoA activation, the S1PR1/VE-cadherin signaling is blocked. S1PR1 controls VE-cadherin expression and EDV via RhoA activation. Moreover, the low expression of S1PR1 correlates with VM and poor prognosis in breast cancer patient. The results show that S1PR1 regulated RhoA activation to accelerate VE-cadherin phosphorylation (Y731), leading to increased EDV and reduced VM in breast cancer. S1PR1 may provide a new thinking direction for antiangiogenic therapy for patients with breast cancer.
    Type of Medium: Online Resource
    ISSN: 2041-4889
    URL: Article
    DOI: 10.1038/s41419-019-1411-x
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2019
    detail.hit.zdb_id: 2541626-1
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  • 8
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    NGAL Expression Is Elevated in Both Colorectal Adenoma–Carcinoma Sequence and Cancer Progression and Enhances Tumorigenesis in Xenograft Mouse Models
    American Association for Cancer Research (AACR) ; 2011
    In:  Clinical Cancer Research Vol. 17, No. 13 ( 2011-07-01), p. 4331-4340
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 17, No. 13 ( 2011-07-01), p. 4331-4340
    Abstract: Purpose: There is growing evidence implicating that neutrophil gelatinase–associated lipocalin (NGAL) plays a role in the development and progression of cancers. However, the effect of NGAL in colorectal carcinoma (CRC) has not been clearly elucidated. In this study, we investigated the role of NGAL in the tumorigenesis and progression of CRC and evaluated the clinical value of NGAL expression. Experimental Design: We examined NGAL expression in 526 colorectal tissue samples, including 53 sets of matched specimens (histologically normal mucosa, adenomas, and carcinomas) using immunohistochemical analysis. In CRCs, correlations between NGAL expression and clinicopathologic parameters were analyzed, and survival analysis was conducted. The role of NGAL was further tested using mouse xenograft models. Results: NGAL expression was elevated during the colorectal adenoma–carcinoma sequence both among the 526 cases (rs = 0.66, P & lt; 0.001) and in the 53 sets of matched specimens (rs = 0.60, P & lt; 0.001). In CRCs, NGAL expression was associated with cancer stage (P = 0.041) and tumor recurrence in stage II patients (P = 0.037). Survival analysis revealed that NGAL expression was an independent prognostic factor for overall survival (HR = 1.84, P = 0.004) and for disease-free survival of stage II patients (HR = 5.88, P = 0.021). In mouse models, the xenografts in cecum and spleen were heavier and more numerous in the group injected with NGAL-overexpressing CRC cells (P & lt; 0.05). Conclusions: NGAL overexpression may promote the tumorigenesis and progression of CRC. Detecting NGAL expression in tumor tissues may be useful for evaluating prognosis of patients with CRC. Clin Cancer Res; 17(13); 4331–40. ©2011 AACR.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-11-0226
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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  • 9
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    Regulation of proliferation, angiogenesis and apoptosis in hepatocellular carcinoma by miR-26b-5p
    Springer Science and Business Media LLC ; 2016
    In:  Tumor Biology Vol. 37, No. 8 ( 2016-8), p. 10965-10979
    Details
    In: Tumor Biology, Springer Science and Business Media LLC, Vol. 37, No. 8 ( 2016-8), p. 10965-10979
    Type of Medium: Online Resource
    ISSN: 1010-4283 , 1423-0380
    URL: Article
    DOI: 10.1007/s13277-016-4964-7
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2016
    detail.hit.zdb_id: 605825-5
    detail.hit.zdb_id: 1483579-4
    SSG: 12
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  • 10
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    Notch4+ cancer stem‐like cells promote the metastatic and invasive ability of melanoma
    Wiley ; 2016
    In:  Cancer Science Vol. 107, No. 8 ( 2016-08), p. 1079-1091
    Details
    In: Cancer Science, Wiley, Vol. 107, No. 8 ( 2016-08), p. 1079-1091
    Abstract: Sphere formation in conditioned serum‐free culture medium supplemented with epidermal growth factor and basic fibroblast growth factor (tumorospheres) is considered useful for the enrichment of cancer stem‐like cells, also known as tumor‐initiating cells. We used a gene expression microarray to investigate the gene expression profile of melanoma cancer stem‐like cells ( MCSLC s). The results showed that MCSLC s highly expressed the following Notch signaling pathway molecules: Notch3 ( NM _008716), Notch4 ( NM _010929), Dtx4 ( NM _172442), and JAG 2 ( NM _010588). Immunofluorescence staining showed tumorosphere cells highly expressed Notch4. Notch4 high B16F10 cells were isolated by FACS , and Western blotting showed that high Notch4 expression is related to the expression of epithelial–mesenchymal transition ( EMT )‐associated proteins. Reduced invasive and migratory properties concomitant with the downregulation of the EMT markers Twist1, vimentin, and VE ‐cadherin and the overexpression of E‐cadherin was observed in human melanoma A375 and MUM ‐2B cells. In these cells, Notch4 was also downregulated, both by Notch4 gene knockdown and by application of the γ‐secretase inhibitor, DAPT . Mechanistically, the re‐overexpression of Twist1 by the transfection of cells with a Twist1 expression plasmid led to an increase in VE ‐cadherin expression and a decrease in E‐cadherin expression. Immunohistochemical analysis of 120 human melanoma tissues revealed a significant correlation between the high expression of Notch4 and the metastasis of melanoma. Taken together, our findings indicate that Notch4+ MCSLC s trigger EMT and promote the metastasis of melanoma cells.
    Type of Medium: Online Resource
    ISSN: 1347-9032 , 1349-7006
    URL: Issue
    URL: Article
    DOI: 10.1111/cas.2016.107.issue-8
    DOI: 10.1111/cas.12978
    Language: English
    Publisher: Wiley
    Publication Date: 2016
    detail.hit.zdb_id: 2115647-5
    detail.hit.zdb_id: 2111204-6
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