Downregulation of the GnT-V gene inhibits metastasis and invasion of BGC823 gastric cancer cells

Huang, Binbin; Sun, Longe; Cao, Jianchun; Zhang, Yunyun; Wu, Qiong; Zhang, Junjie; Ge, Yanli; Fu, Liu; Wang, Zhirong

doi:10.3892/or.2013.2373

Cited by 24 publications

(17 citation statements)

References 37 publications

(45 reference statements)

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“…For example, a close association was identified between GnT-V activity and tumor invasiveness in the sera of patients with HCC (19). Additionally, in vitro GnT-V-knockdown may decrease the invasive ability of the BGC823 gastric cancer cell line (11). Notably, the present results demonstrated that suppressing the expression of GnT-V markedly reduced cell-to-cell adherence and the invasive abilities of the SMMC-7721/R cells.…”

Section: Discussionsupporting

confidence: 56%

“…N-glycosyltransferase-V (GnT-V), as a key member of the glycosyltransferase family, is closely associated with the proliferation, migration and invasion of cancer cells (6)(7). Previous studies reported that GnT-V is commonly overexpressed in various advanced tumor types, including prostate cancer, oral squamous cell carcinoma, colorectal and breast cancer, gastric cancer cells and ovarian mucinous cancer (8)(9)(10)(11)(12)(13). Notably, previous studies identified that the downregulation of GnT-V markedly suppressed the proliferation and migration of tumor cells, and induced cell apoptosis (11,14,15).…”

Section: Introductionmentioning

confidence: 99%

“…Previous studies reported that GnT-V is commonly overexpressed in various advanced tumor types, including prostate cancer, oral squamous cell carcinoma, colorectal and breast cancer, gastric cancer cells and ovarian mucinous cancer (8)(9)(10)(11)(12)(13). Notably, previous studies identified that the downregulation of GnT-V markedly suppressed the proliferation and migration of tumor cells, and induced cell apoptosis (11,14,15). Preliminary experiments in our laboratory demonstrated that GnT-V is highly expressed in SMMC7721 cells (unpublished data), although the effect of reducing the expression of GnT-V on the proliferation, migration and invasion of SMMC7721/R cells remains to be fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

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Effect of GnT-V knockdown on the proliferation, migration and invasion of the SMMC7721/R human hepatocellular carcinoma drug-resistant cell line

Zhang

et al. 2015

Molecular Medicine Reports

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Hepatocellular carcinoma (HCC) is a commonly occurring malignant tumor, with a high incidence rate. The present study aimed to investigate the effect of knocking down the N‑glycosyltransferase‑V (GnT‑V) protein on the proliferation, migration and invasion of the human HCC drug‑resistant cell line, SMMC7721/R. SMMC7721/R cells with GnT‑V‑knockdown (SMMC‑7721/R‑GnT‑V) were constructed using the method of lentiviral transfection. The expression of GnT‑V was assessed using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blotting. Cell proliferation was determined using an MTT assay, and the extent of cellular apoptosis was assessed using flow cytometric analysis. Additionally, the metastatic ability of the cells in vitro was analyzed using cell adhesion and invasion assays. Western blotting was used to investigate the protein expression levels of caspase‑3, caspase‑9, Bcl‑2, Bax, matrix metalloproteinase (MMP)‑2 and MMP‑9, and RT‑qPCR was used to determine the mRNA expression levels of the genes for the breast cancer resistance protein and P‑glycoprotein in the SMMC‑7721/R cells. Taken together, the results of the present study revealed that the knockdown of GnT‑V significantly suppressed the proliferation, migration and invasion (P<0.05) of the SMMC‑7721/R cells. Furthermore, the possible mechanism underlying these phenomena may be associated with the induction of mitochondria‑mediated apoptosis, inhibition of the degradation of the extracellular matrix and an enhancement of the drug-sensitivity. GnT‑V‑knockdown may therefore be used to treat drug‑resistant HCC in the future.

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Section: Discussionsupporting

confidence: 56%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effect of GnT-V knockdown on the proliferation, migration and invasion of the SMMC7721/R human hepatocellular carcinoma drug-resistant cell line

Zhang

et al. 2015

Molecular Medicine Reports

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“…This structure was catalyzed by UDP-N-acetylglucosamine: α-6-D-manno-side β1–6-N-acetylglucosaminyltransferase (EC2.4.1.155) which was known as GnT-V. Expression levels of β1,6-GlcNAc branched N-glycan and GnT-V were associated with metastasis in human digestive cancers such as colorectal carcinoma and gastric cancer (Seelentag et al, 1998; Kim et al, 2008; Huang et al, 2013; Huang, B. et al, 2014). In our previous studies, we have found this glycoform was increased in epithelial mesenchymal transition (EMT) process of Huh7 HCC cell and it might be a metastasis-promoting glycoform in HCC (Li, S. et al, 2013).…”

Section: Resultsmentioning

confidence: 99%

Assessment of Hepatocellular Carcinoma Metastasis Glycobiomarkers Using Advanced Quantitative N-glycoproteome Analysis

Liu

Shang

et al. 2017

Front. Physiol.

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Hepatocelluar carcinoma (HCC) is one of the most common malignant tumors with high incidence of metastasis. Glycosylation is involved in fundamental molecular and cell biology process occurring in cancer including metastasis formation. In this study, lectin microarray, lectin blotting, lectin affinity chromatography and tandem 18O stable isotope labeling coupled with liquid chromatography-mass spectrometer (LC-MS) analysis were applied to quantify the changes in N-glycosite occupancy for HCC metastasis serum. Firstly, lectin microarray was used to screen glycoforms and Phaseolus vulgaris Leucoagglutinin (PHA-L) reactive structure (β1,6-GlcNAc branched N-glycan) was found to be increased significantly in HCC patients with metastasis compared with those with non-metastasis. Then, PHA-L affinity glycoproteins were enriched followed by N-glycosite occupancy measurement with strategy of tandem 18O stable isotope labeling. 11 glycoproteins with significantly changed N-glycosite occupancy were identified, they were associated with cell migration, invasion and adhesion through p38 mitogen-activated protein kinase signaling pathway and nuclear factor kappa B signaling pathway. Quantification of N-glycosite occupancy for PHA-L reactive glycoproteins could help to discover important glycoproteins of potential clinically significance in terms of HCC etiology. Also, understanding of N-glycosite occupancy alterations will aid the characterization of molecular mechanism of HCC metastasis as well as establishment of novel glycobiomarkers.

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“…Epithelial–mesenchymal transition is related to cancer invasion and metastasis [27,28]. TGF-β1 may induce EMT by down-regulating E-cadherin and up-regulating vimentin in GC cells [29].…”

Section: Resultsmentioning

confidence: 99%

Epigenetic silencing of DACH1 induces the invasion and metastasis of gastric cancer by activating TGF‐β signalling

Herman

et al. 2014

J Cellular Molecular Medi

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Gastric cancer (GC) is the fourth most common malignancy in males and the fifth most common malignancy in females worldwide. DACH1 is frequently methylated in hepatic and colorectal cancer. To further understand the regulation and mechanism of DACH1 in GC, eight GC cell lines, eight cases of normal gastric mucosa, 98 cases of primary GC and 50 cases of adjacent non-tumour tissues were examined. Methylation-specific PCR, western blot, transwell assay and xenograft mice were used in this study. Loss of DACH1 expression correlated with promoter region methylation in GC cells, and re-expression was induced by 5-Aza-2′-deoxyazacytidine. DACH1 is methylated in 63.3% (62/98) of primary GC and 38% (19/50) of adjacent non-tumour tissues, while no methylation was found in normal gastric mucosa. Methylation of DACH1 correlated with reduced expression of DACH1 (P < 0.01), late tumour stage (stage III/IV) (P < 0.01) and lymph node metastasis (P < 0.05). DACH1 expression inhibited epithelial–mesenchymal transition and metastasis by inhibiting transforming growth factor (TGF)-β signalling and suppressed GC cell proliferation through inducing G2/M phase arrest. The tumour size is smaller in DACH1-expressed BGC823 cell xenograft mice than in unexpressed group (P < 0.01). Restoration of DACH1 expression also sensitized GC cells to docetaxel. These studies suggest that DACH1 is frequently methylated in human GC and expression of DACH1 was controlled by promoter region methylation. DACH1 suppresses GC proliferation, invasion and metastasis by inhibiting TGF-β signalling pathways both in vitro and in vivo. Epigenetic silencing DACH1 may induce GC cells' resistance to docetaxel.

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Downregulation of the GnT-V gene inhibits metastasis and invasion of BGC823 gastric cancer cells

Cited by 24 publications

References 37 publications

Effect of GnT-V knockdown on the proliferation, migration and invasion of the SMMC7721/R human hepatocellular carcinoma drug-resistant cell line

Effect of GnT-V knockdown on the proliferation, migration and invasion of the SMMC7721/R human hepatocellular carcinoma drug-resistant cell line

Assessment of Hepatocellular Carcinoma Metastasis Glycobiomarkers Using Advanced Quantitative N-glycoproteome Analysis

Epigenetic silencing of DACH1 induces the invasion and metastasis of gastric cancer by activating TGF‐β signalling

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