Investigation of the sensitivities of distinct gastric cancer cells to parvovirus H‐1 induced cytotoxicity

Ran, Zhi Hua; Liu, Jiong; Feng, Ying; Zou, Jian; Xiao, Shu Dong

doi:10.1111/j.1443-9573.2004.00163.x

Cited by 6 publications

(7 citation statements)

References 18 publications

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“…In contrast, the NS1 transduction of MKN28 cells was not associated with a significant decrease of their tumorigenicity, as compared to parental or empty vector‐transfected controls. A parallel can be drawn between these results and our previous study showing that MKN28 cells can be distinguished from MKN45 and SGC7901 cells by their much lower sensitivity to the toxic activity of parvovirus H‐1 12 …”

Section: Discussionsupporting

confidence: 83%

“…In contrast, no difference in growth rate was found in the MKN28‐derived transfectants. These data may be correlated with the insensitivity of the parental cell line to infection with parvovirus H‐1 described previously 12 . In addition, NS1 expression in MKN45 and SGC7901 cells correlated with a striking suppression of their capacity to form tumors after xenografting into immunodeficient mice.…”

Section: Discussionsupporting

confidence: 81%

“…We previously compared the cytotoxic effects of parvovirus H‐1 on different gastric cancer cell lines and demonstrated that poorly differentiated cells were more sensitive to virus attack. This correlated with an enhanced capacity of poorly differentiated gastric cancer cells for NS1 protein production and accumulation 12 . In the present study, an eukaryotic NS1‐expressing recombinant plasmid, pcDNA3.1‐NS1, was successfully constructed and used to study the effect of parvovirus H‐1 NS1 on the tumorigenicity of distinct differentiated gastric cancer cell lines, in connection with the expression of the cell adhesion molecule CD44.…”

Section: Introductionmentioning

confidence: 94%

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Effect of the parvovirus H‐1 non‐structural protein NS1 on the tumorigenicity of human gastric cancer cells

Wang

Liu

Zheng

et al. 2012

J of Digest Diseases

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OBJECTIVE: To investigate the in vivo oncosuppressive effect of the non‐structural protein NS1 of parvovirus H‐1 on human gastric cancer cell lines. METHODS: Recombinant plasmid pcDNA3.1‐NS1 containing the complete NS1 gene of parvovirus H‐1 was constructed and characterized by restriction enzyme digestion and sequence analysis. The human gastric cancer cell lines MKN28, SGC7901 and MKN45 were stably transfected with empty or recombinant plasmids. NS1 gene transcription and protein expression in the latter transfectants were verified by reverse transcriptase polymerase chain reaction and Western blot, respectively. The oncosuppressive effect of the parvoviral protein NS1 on the gastric cancer cell lines was tested by comparing the tumorigenicity of empty and recombinant vector‐transfected cells in nude mice. RESULTS: Well differentiated gastric cancer cells (MKN28) transfected with either empty plasmid or pcDNA3.1‐NS1 were tumorigenic in nude mice. Moderately (SGC7901) and poorly (MKN45) differentiated gastric cancer cells transfected with empty plasmid were also tumorigenic, but no tumor resulted from the injection when they were transfected with pcDNA3.1‐NS1. This NS1‐associated suppression of SGC7901 and MKN45 tumors correlated with the decreased percentage of CD44 positive cells. CONCLUSIONS: NS1 expression in poorly differentiated gastric cancer cells prevents them from forming tumors, perhaps by impairing the stem‐like phenotype. The parvoviral NS1 protein warrants further investigation for its therapeutic potential against cancer.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionsupporting

confidence: 81%

Section: Introductionmentioning

confidence: 94%

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Effect of the parvovirus H‐1 non‐structural protein NS1 on the tumorigenicity of human gastric cancer cells

Wang

Liu

Zheng

et al. 2012

J of Digest Diseases

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“…Although we observed that KLK12 had a similar effect on cell proliferation and migration in all three cell lines, AGS cells displayed a lower degree of differentiation in the S phase (Ran et al, 2004). This is of relevance considering that Helicobacter pylori can easily adhere to and invade human gastric epithelial cells.…”

Section: Discussionmentioning

confidence: 59%

Kallikrein 12 downregulation reduces AGS gastric cancer cell proliferation and migration

2016

Genet. Mol. Res.

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ABSTRACT. Abnormal expression of the kallikrein (KLK) family of serine proteases closely correlates with onset, progression, and prognosis of endocrine gland-related malignant tumors. The aim of this study was to evaluate how downregulation of KLK12 influenced cell cycle and proliferation of the AGS gastric cancer cell line. KLK12 was detected by western blot in GES-1 normal gastric epithelial and AGS cells. AGS cells were transfected with KLK12 siRNA, a negative control siRNA, or subjected to a mock transfection, following which, we assessed mRNA and protein levels, cell proliferation, cell migration, and cell cycle progression. We found that KLK12 levels were significantly higher in AGS cells than in GES-1 cells. Transfection of AGS cells with KLK12 siRNA led to downregulation of KLK12 mRNA and protein expression, reduced cell proliferation (0.47 ± 0.03 vs 0.92 ± 0.04, P < 0.01), and lower cell counts (3.92 ± 0.25 x 10 5 vs 5.47 ± 0.50 x 10 5 , P < 0.01) with respect to the negative control. We observed that KLK12 siRNA increased the number of AGS cells in G0/G1 and reduced those in S phase. Furthermore, downregulation of KLK12 in AGS cells decreased their ability to penetrate the membrane in a migration assay (P < 0.05).In conclusion, KLK12 siRNA inhibited the proliferation and migration of AGS gastric cancer cells and caused their arrest in the G0/G1 phase of the cell cycle.

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“…For example, SGC‐7901 (moderately differentiated) and MKN‐28 (well differentiated) are two distinctly differentiated gastric cancer cell lines and they could respond differently upon the exposure to anticancer compounds. It has been shown that six gastric cancer cell lines had different sensitivities for the cytotoxic effects of parvovirus H‐1 (Ran et al . 2004).…”

Section: Resultsmentioning

confidence: 99%

The Inhibitory Effects of Pure Black Tea Theaflavins on the Growth of Four Selected Human Cancer Cells

Wang¹,

Z²,

Huang³

et al. 2011

Journal of Food Biochemistry

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The growth inhibition and cytotoxic effects of theaflavins mixture and pure theaflavins [theaflavin, theaflavins-3-gallate, theaflavins-3′-gallate and theaflavin-3, 3′-digallate] from black tea on human liver cancer HepG2 cells, gastric cancer SGC-7901 cells, lung cancer A549 cells and acute promyelocytic leukemia K562 cells were investigated. The four major theaflavins were obtained from enzymatically oxidized catechins mixture using preparative high-performance liquid chromatography (HPLC). The purity and the structures of the isolated compounds were confirmed by Journal of Food Biochemistry ISSN 1745-4514

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Investigation of the sensitivities of distinct gastric cancer cells to parvovirus H‐1 induced cytotoxicity

Cited by 6 publications

References 18 publications

Effect of the parvovirus H‐1 non‐structural protein NS1 on the tumorigenicity of human gastric cancer cells

Effect of the parvovirus H‐1 non‐structural protein NS1 on the tumorigenicity of human gastric cancer cells

Kallikrein 12 downregulation reduces AGS gastric cancer cell proliferation and migration

The Inhibitory Effects of Pure Black Tea Theaflavins on the Growth of Four Selected Human Cancer Cells

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