2018
DOI: 10.3233/cbm-181466
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Downregulated GBX2 gene suppresses proliferation, invasion and angiogenesis of breast cancer cells through inhibiting the Wnt/β-catenin signaling pathway

Abstract: The study has made an attempt to provide evidence to the idea that GBX2 gene silencing has an inhibition effect on the proliferation, invasion and angiogenesis of the breast cancer cells by inhibiting the activation of the Wnt/β-catenin signaling pathway.

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Cited by 14 publications
(13 citation statements)
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“…Our findings are in line with studies in colon cancer indicating a positive relationship between MSI proteins and CD44 [33,34]. • GBX2, a key marker for stem cell progenitors [26], is also downregulated after MSI knockdown. Its downregulation is known to inhibit proliferation [26], prompting further proliferation analyses (see below).…”
supporting
confidence: 91%
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“…Our findings are in line with studies in colon cancer indicating a positive relationship between MSI proteins and CD44 [33,34]. • GBX2, a key marker for stem cell progenitors [26], is also downregulated after MSI knockdown. Its downregulation is known to inhibit proliferation [26], prompting further proliferation analyses (see below).…”
supporting
confidence: 91%
“…Hence, we quantified several stem cell markers to understand the effect of MSI knockdown on BCSCs: CD44, a key stemness-associated marker protein [25], was downregulated by more than 20% (p < 0.05) in flow cytometric analysis ( Figure 2B, representative graph in Figure 2C). GBX2, another stem-cell-associated molecule [26], was downregulated 40% compared to non-MSI-knockdown controls when quantified by qPCR (p < 0.05, Figure 2D). Finally, vimentin, a major cytoskeletal element linked to the BCSC phenotype [27], showed lower mRNA expression in MSI-knockdown cells when compared to controls (p < 0.01, Figure 2D), a result confirmed using Western blots (Supplementary Figure S3).…”
Section: Breast Cancer Stem Cell Markers Are Downregulated After Msi mentioning
confidence: 99%
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“…For example, it was documented that GBX2 exhibits high levels in prostate cancer in contrast to normal prostate epithelial cells, and GBX2 expression silencing restrains cell cloning efficiency and tumorgenetic ability . In breast cancer, it has been revealed that down‐regulation of GBX2 gene could suppress tumor cell proliferation, invasion and angiogenesis . In sum, such evidence provides good theoretical support for the present study, and illustrates that GBX2 may play a cancer‐promoting effect on the progression and tumorigenicity of lung adenocarcinoma.…”
Section: Discussionsupporting
confidence: 79%
“…It is expressed in the forebrain during vertebrate brain development, which helps to locate the midbrain–hindbrain boundary that controls the progression of adjacent brain areas in vertebrate embryos . In recent studies, it has been reported that GBX2 has connections with the progression of certain cancers, such as breast cancer and prostatic cancer . Moreover, it was well established that GBX2 could be seen as a direct target of microRNA‐4497, and its expression is reversely regulated by miR‐4497 to participate in cell viability and apoptosis in laryngeal squamous cell carcinoma .…”
Section: Introductionmentioning
confidence: 99%