Vasohibin 2 promotes human luminal breast cancer angiogenesis in a non-paracrine manner via transcriptional activation of fibroblast growth factor 2

Tu, Min; Lü, Cheng; Lv, Nan; Wei, Jishu; Lu, Zipeng; Xi, Chunhua; Chen, Jianmin; Guo, Feng; Jiang, Kuirong; Li, Qiang; Wu, Junli; Song, Guoxin; Wang, Shui; Gao, Wentao

doi:10.1016/j.canlet.2016.09.031

Cited by 11 publications

(12 citation statements)

References 32 publications

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“…Matrigel (60 μL/well) was seeded into the 96‐well plates for a 1 hour incubation at 37℃. Subsequently, human umbilical vein endothelial cells (HUVECs) were inoculated at 2 × 10 5 cells/mL and treated according to grouping . After 8 hours, an inverted phase contrast microscope (IX70; Olympus, Tokyo, Japan) was adopted to analyze the tubes formed.…”

Section: Methodsmentioning

confidence: 99%

Retracted: PRC1 gene silencing inhibits proliferation, invasion, and angiogenesis of retinoblastoma cells through the inhibition of the Wnt/β‐catenin signaling pathway

Liao

Yin

Deng

et al. 2019

J of Cellular Biochemistry

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Retinoblastoma is an ocular malignancy occurring in childhood. The current study evaluates the ability of silenced PRC1 on retinoblastoma cell proliferation, and angiogenesis via the Wnt/β‐catenin signaling pathway. A total of 36 cases of retinoblastoma tissues (n = 36) and normal retinal tissues (n = 10) were selected in the current study. Retinoblastoma cells presenting with the high PRC1 messenger RNA (mRNA) expression were selected among the WERI‐Rb‐1, HXO‐RB44, Y79, SO‐Rb50, and SO‐Rb70 cells lines, and were transfected with siRNA‐PRC1 and LiCl (the activator of the Wnt/β‐catenin pathway). The expressions of PRC1, VEGF, Wnt1, β‐catenin, CyclinD1, extent of β‐catenin, and GSK‐3β phosphorylation were evaluated. Cell proliferation, cell‐cycle distribution, and cell invasion of retinoblastoma cells were evaluated by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay, flow cytometry, and Transwell assay. The angiogenesis of retinoblastoma cells was detected by tube formation assay. HXO‐RB44 and WERI‐Rb‐1 cells were selected owing to the highest PRC1 mRNA expression. Meanwhile, PRC2 gene silencing presented lower expression levels of PRC1, VEGF, Wnt1, β‐catenin, CyclinD1, extent of β‐catenin and GSK‐3β phosphorylation, decreased proliferation and invasion abilities, extended G0/G1 phase, and shortened S and G2/M phases of HXO‐RB44 and WERI‐Rb‐1 cells, suggesting the silenced PRC2 inactivated Wnt/β‐catenin pathway, so as to further restrain the retinoblastoma cell proliferation, invasion, and angiogenesis. These results support the view that PRC1 gene silencing could suppress the proliferation, and angiogenesis of retinoblastoma cells by repressing the Wnt/β‐catenin pathway.

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Section: Methodsmentioning

confidence: 99%

Retracted: PRC1 gene silencing inhibits proliferation, invasion, and angiogenesis of retinoblastoma cells through the inhibition of the Wnt/β‐catenin signaling pathway

Liao

Yin

Deng

et al. 2019

J of Cellular Biochemistry

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“…Several studies have shown that VASH2 is highly expressed in HCC, breast cancer, and ovarian cancer, and that there is a close association between VASH2 expression and EMT in these malignancies. 13,14,18 However, the role of VASH2 in the EMT process of PC cells remains unclear. In this study, we found that VASH2 expression is significantly elevated in PC tissues and VASH2 promotes EMT in PC cell lines, indicating that VASH2 Overexpression of VASH2 has also been demonstrated to accelerate malignant transformation and promote gemcitabine resistance in PC.…”

Section: Discussionmentioning

confidence: 99%

Vasohibin 2 promotes malignant behaviors of pancreatic cancer cells by inducing epithelial‐mesenchymal transition via Hedgehog signaling pathway

Zhang

Xue²,

Zhao

et al. 2018

Cancer Medicine

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BackgroundBased on previous findings, we hypothesized that Vasohibin 2 (VASH2) protein may induce epithelial‐mesenchymal transition (EMT) of pancreatic cancer (PC) cells by promoting the malignant behaviors of these cells. The present study aimed to test this hypothesis and explore the possible mechanisms involved.MethodsThe expression of VASH2 in PC tissues and cell lines was detected by quantitative real‐time PCR and Western blot. PC cells with overexpression or knockdown of VASH2 were used to examine the involvement of VASH2 in EMT by detecting the expression of epithelial (E‐cadherin) and mesenchymal (vimentin) markers and EMT‐related transcription factor ZEB1/2, in gemcitabine resistance and tumor cell invasion by apoptosis and invasion assays, and in cancer stem cell‐like phenotypes by detecting the proportion of CD24+CD44+ and side population (SP) cells in PC cells with flow cytometry. The impact of VASH2 overexpression and knockdown on components of the Hedgehog signaling pathway was also assessed.ResultsWe found that VASH2 was highly expressed in PC tissues and cells. It promoted the EMT of PC cells by altering ZEB1/2 expression. VASH2 also stimulated invasion and chemotherapeutic resistance of PC cells and increased the proportion of cancer stem‐like cells in PC cells. VASH2 did so by upregulating the expression of multiple molecules in the Hedgehog signaling pathway of PC cells.ConclusionVASH2 promotes malignant behaviors of PC cells by inducing EMT via activation of the Hedgehog signaling pathway.

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“…In 2015, Kim et al reported that VASH2 was positively correlated with clinical stage, tumor proliferation and micro vessel density (MVD), as well as poor outcome of pancreatic cancer patients (9). For BC cancer, Tu et al reported that VASH2 could promote proliferation and EMT of BC cells (12,13). But, the role of VASH2 in drug resistance of BC cells has not been reported.…”

Section: Discussionmentioning

confidence: 99%

“…It is reported that VASH2 can play important roles in proliferation, angiogenesis and epithelial mesenchymal transition (EMT) of hepatocellular carcinoma, ovarian adenocarcinoma, pancreatic ductal adenocarcinoma and endometrial cancer cells (7)(8)(9)(10)(11). In BC, it has been reported that VASH2 could promote EMT and proliferation of BC cells through in vivo and in vitro experiments (12,13). However, its role in drug resistance of BC is still unknown.…”

Section: Introductionmentioning

confidence: 99%

Vasohibin2 promotes adriamycin resistance of breast cancer cells through regulating ABCG2 via AKT signaling pathway

et al. 2017

Molecular Medicine Reports

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As a well‑known angiogenic factor in different histology and pathological conditions, the pro‑progressive role of vasohibin2 (VASH2) has been reported in various types of tumors. However, its role in drug resistance of breast cancer has not been reported so far. The present study demonstrated that MCF‑7 cells with increased expression of VASH2 demonstrate stronger adriamycin (ADM) resistance compared with MDA‑MB‑231 cells with decreased expression of VASH2. Overexpression of VASH2 in MDA‑MB‑231 cells increased ADM resistance and silencing VASH2 in MCF‑7 cells inhibited ADM resistance. Furthermore, in newly established ADM resistant cell lines, VASH2 was significantly upregulated. These results revealed the promotive role of VASH2 in the ADM resistance of breast cancer cells. In addition, overexpression of VASH2 in MDA‑MB‑231 cells significantly upregulated ATP‑binding cassette sub‑family G member 2 (ABCG2), however silencing VASH2 in MCF‑7 cells inhibited ABCG2 significantly. Silencing ABCG2 abrogated increase of ADM resistance induced by VASH2 overexpression in MDA‑MB‑231 cells. This proved that VASH2 induced ADM resistance through promoting expression of ABCG2, at least in part. Further study regarding the underlying molecular mechanism demonstrated that VASH2 promoted ABCG2 via the protein kinase B (AKT) signaling pathway. Overall, VASH2 may promote drug resistance of breast cancer cells through regulating ABCG2 via the AKT signaling pathway. This suggests a novel therapeutic target to inhibit drug resistance in breast cancer, for a more efficient therapeutic outcome.

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Vasohibin 2 promotes human luminal breast cancer angiogenesis in a non-paracrine manner via transcriptional activation of fibroblast growth factor 2

Cited by 11 publications

References 32 publications

Retracted: PRC1 gene silencing inhibits proliferation, invasion, and angiogenesis of retinoblastoma cells through the inhibition of the Wnt/β‐catenin signaling pathway

Retracted: PRC1 gene silencing inhibits proliferation, invasion, and angiogenesis of retinoblastoma cells through the inhibition of the Wnt/β‐catenin signaling pathway

Vasohibin 2 promotes malignant behaviors of pancreatic cancer cells by inducing epithelial‐mesenchymal transition via Hedgehog signaling pathway

Vasohibin2 promotes adriamycin resistance of breast cancer cells through regulating ABCG2 via AKT signaling pathway

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