Knockdown of RAGE inhibits growth and invasion of gastric cancer cells

Xu, Xiao; Abuduhadeer, Xiaokaiti; Zhang, W.B.; Li, T.; Gao, Hua; Wang, Y.H.

doi:10.4081/ejh.2013.e36

Cited by 38 publications

(30 citation statements)

References 30 publications

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“…In gastric cancer, knockdown of RAGE reduced the proliferation and invasion of cells, implying that RAGE promotes the proliferation and invasion of cancer cells (Xu et al, 2013;Wang et al, 2015). In this study, we constructed OS U-2OS cells that overexpressed RAGE by transfecting a recombinant plasmid into the cells, and determined the function of RAGE in OS cells.…”

Section: Discussionmentioning

confidence: 99%

Receptor for advanced glycation end-products (RAGE) is overexpressed in human osteosarcoma and promotes the proliferation of osteosarcoma U-2OS cells in vitro

Zhang¹,

Jin²,

Cf³

et al. 2016

Genet. Mol. Res.

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ABSTRACT. Osteosarcoma (OS) is an aggressive cancer of the long bones, and usually affects children and young adults. The receptor for advanced glycation end-products (RAGE) has recently been recognized as an oncogenic receptor that binds to different ligands, and promotes the progression of various cancers. However, little is known about the association between RAGE and the pathogenesis of OS. In this study, we first examined the expression of RAGE in OS tissues using immunohistochemical staining, western blotting, and reverse transcription quantitative polymerase chain reaction. We then determined the influence of the overexpressed RAGE on the proliferation of U-2OS cells in vitro. The results showed that RAGE was overexpressed in OS tissues compared with peritumor tissues, at both the mRNA and protein levels, and there was a significant association between overexpressed RAGE and clinicopathological characteristics, such as clinical stage and distant metastasis. Moreover, the overexpression of RAGE in U-2OS cells significantly promoted their proliferation in vitro. In conclusion, this study indicated that RAGE is overexpressed in OS tissue and promotes the proliferation of U-2OS cells. These data imply that RAGE promotes the growth of OS, and is a potential diagnostic biomarker and therapeutic target for the disorder.

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Section: Discussionmentioning

confidence: 99%

Receptor for advanced glycation end-products (RAGE) is overexpressed in human osteosarcoma and promotes the proliferation of osteosarcoma U-2OS cells in vitro

Zhang¹,

Jin²,

Cf³

et al. 2016

Genet. Mol. Res.

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“…Furthermore, blockade of RAGE signaling have been used to inhibit tumor growth, invasion and angiogenesis in a variety of cancers (9-12). One of the earliest reports to demonstrate the therapeutic efficacy of this approach was in gliomas where blockade of RAGE interaction with HMGB1 was shown to inhibit tumor growth and invasion (13).…”

Section: Introductionmentioning

confidence: 99%

RAGE Expression in Tumor-Associated Macrophages Promotes Angiogenesis in Glioma

et al. 2014

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Interaction of RAGE with its ligands can promote tumor progression, invasion and angiogenesis. Although blocking RAGE signaling has been proposed as a potential anti-cancer strategy, functional contributions of RAGE expression in the tumor microenvironment (TME) has not been investigated in detail. Here, we evaluated the effect of genetic depletion of RAGE in TME on the growth of gliomas. In both invasive and non-invasive glioma models, animal survival was prolonged in RAGE knockout (Ager−/−) mice. However, the improvement in survival in Ager−/− mice was not due to changes in tumor growth rate but rather to a reduction in tumor-associated inflammation. Furthermore, RAGE ablation in the TME abrogated angiogenesis by downregulating the expression of pro-angiogenic factors which prevented normal vessel formation, thereby generating a leaky vasculature. These alterations were most prominent in non-invasive gliomas, where the expression of VEGF and pro-inflammatory cytokines were also lower in tumor-associated macrophages (TAM) in Ager−/− mice. Interestingly, reconstitution of Ager−/− TAM with wild-type microglia or macrophages normalized tumor vascularity. Our results establish that RAGE signaling in glioma-associated microglia and TAM drives angiogenesis, underscoring the complex role of RAGE and its ligands in gliomagenesis.

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“…[10][11][12][13][14][15][16]. In vitro and clinical studies suggest that RAGE activation is associated with proliferation, migration, and invasion of cancer cells [17].…”

Section: Introductionmentioning

confidence: 99%