Serial observations on an orthotopic gastric cancer model constructed using improved implantation technique

Li, Yan; Li, Bo; Xiang, Chun-Ping; Li, Yuanyuan; Wu, Xiaoling

doi:10.3748/wjg.v17.i11.1442

Cited by 10 publications

(4 citation statements)

References 17 publications

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“…Each tumor piece was placed into a small tissue pocket formed in the middle wall of the greater curvature of the stomach beneath the serosa in another nude mouse, and fixed using a purse string suture with 7-0 absorbable sutures. After tumor implantation, the stomach was relocated into the abdominal cavity followed by abdominal closure (Li et al, 2011 ) and tumors were allowed to grow for 8 weeks. All procedures were performed under anesthesia with ketamine (50 mg/kg)/midazolam (10 mg/kg) following an approved protocol in conformity with institutional guidelines for the care and use of laboratory animals in Shanghai Jiao Tong University School of Medicine.…”

Section: Methodsmentioning

confidence: 99%

SENP3 regulates the global protein turnover and the Sp1 level via antagonizing SUMO2/3-targeted ubiquitination and degradation

et al. 2015

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SUMOylation is recently found to function as a targeting signal for the degradation of substrates through the ubiquitin-proteasome system. RNF4 is the most studied human SUMO-targeted ubiquitin E3 ligase. However, the relationship between SUMO proteases, SENPs, and RNF4 remains obscure. There are limited examples of the SENP regulation of SUMO2/3-targeted proteolysis mediated by RNF4. The present study investigated the role of SENP3 in the global protein turnover related to SUMO2/3-targeted ubiquitination and focused in particular on the SENP3 regulation of the stability of Sp1. Our data demonstrated that SENP3 impaired the global ubiquitination profile and promoted the accumulation of many proteins. Sp1, a cancer-associated transcription factor, was among these proteins. SENP3 increased the level of Sp1 protein via antagonizing the SUMO2/3-targeted ubiquitination and the consequent proteasome-dependent degradation that was mediated by RNF4. De-conjugation of SUMO2/3 by SENP3 attenuated the interaction of Sp1 with RNF4. In gastric cancer cell lines and specimens derived from patients and nude mice, the level of Sp1 was generally increased in parallel to the level of SENP3. These results provided a new explanation for the enrichment of the Sp1 protein in various cancers, and revealed a regulation of SUMO2/3 conjugated proteins whose levels may be tightly controlled by SENP3 and RNF4.

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Section: Methodsmentioning

confidence: 99%

SENP3 regulates the global protein turnover and the Sp1 level via antagonizing SUMO2/3-targeted ubiquitination and degradation

et al. 2015

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“…Orthotopic gastric cancer model was made according to publication in literature [ 43 ]. SGC7901 cells of 1×10 7 were injected subcutaneously into the 6-wk-old Balb/c nu-nu mice.…”

Section: Methodsmentioning

confidence: 99%

De-SUMOylation of FOXC2 by SENP3 promotes the epithelial-mesenchymal transition in gastric cancer cells

et al. 2014

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The impact of cellular oxidative stress in promoting the epithelial-mesenchymal transition (EMT) has been noticed. Our previous study shows that SENP3, a redox-sensitive SUMO2/3-specific protease, accumulates in a variety of cancers, but whether SENP3 and SUMOylation involve in the regulation of EMT is unclear. The present study uncovers a novel role of SENP3 in promoting the EMT process in gastric cancer via regulating an EMT-inducing transcription factor, forkhead box C2 (FOXC2). We demonstrate that the expression of mesenchymal marker genes and cell migration ability are enhanced in SENP3-overexpressing gastric cancer cells and attenuated in SENP3-knockdown cells. A nude mouse model and a set of patient's specimens suggest the correlation between SENP3 and gastric cancer metastasis. Biochemical assays identify FOXC2 as a substrate of SENP3. Meanwhile N-cadherin is verified as a target gene of FOXC2, which is transcriptionally activated by a SUMO-less FOXC2. Additionally, reactive oxygen species-induced de-SUMOylation of FOXC2 can be blocked by silencing endogenous SENP3. In conclusion, SENP3, which is increased in gastric cancer cells, potentiates the transcriptional activity of FOXC2 through de-SUMOylation, in favor of the induction of specific mesenchymal gene expression in gastric cancer metastasis.

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“…Before sugery, the female mice were administered with rhabarber and glauber to further reduce the immunity and improve the rate of tumor formation. The surgical procedure of gastric orthotopic transplantation was performed as previously reported(41). Briefly, subcutaneous GC tissue pieces (~2.0 cm x 2.0 cm x 1.0 cm) were harvested and minced into small pieces (~1 mm 3 ).…”

mentioning

confidence: 99%

Toosendanin suppresses oncogenic phenotypes of human gastric carcinoma SGC-7901 cells partly via miR-200a-mediated downregulation of β-catenin pathway

Wang

Huang

Zhang

et al. 2017

International Journal of Oncology

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Aberrant activation of β-catenin signaling due to low expression of miR‑200a is found in gastric carcinoma (GC) tissues promoting GC evolution. Toosendanin (TSN) has exhibited antitumor effects on various human cancer cells, but its influence on GC is largely unidentified. The potential roles of TSN on GC cells were examined and it was found that TSN inhibited growth, migration, invasion and TGF‑β1-induced epithelial-mesenchymal transition (EMT) and induced cell cycle arrest and apoptosis in SGC‑7901 cells which were most sensitive to TSN among various GC cell lines. TSN also inactivated β-catenin pathway in SGC‑7901 cells and the above effects were reversed following induction of β-catenin overexpression. Moreover, TSN facilitated the level of miR‑200a which targets β-catenin and miR‑200a silencing attenuated the antitumor effects of TSN on SGC‑7901 cells. Nonetheless, knockdown of miR‑200a did not relieve the suppressive effects of TSN on p‑AKT, p‑ERK and p‑GSK3β which were upstream regulators of β-catenin. In addition, TSN administration inhibited growth and liver metastasis of orthotopically implanted SGC‑7901 tumors in vivo through miR‑200a‑mediated β-catenin pathway. Our data suggest that TSN may suppress oncogenic phenotypes of human GC cells partly via miR‑200a/β-catenin axis. Hence, TSN may have a promising chemotherapeutic activity for GC therapy.

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Serial observations on an orthotopic gastric cancer model constructed using improved implantation technique

Abstract: A gastric cancer model is established, which can simulate the clinical tumor behavior and provide experimental carrier for clinical trials of gastric cancer treatment.

Cited by 10 publications

References 17 publications

SENP3 regulates the global protein turnover and the Sp1 level via antagonizing SUMO2/3-targeted ubiquitination and degradation

SENP3 regulates the global protein turnover and the Sp1 level via antagonizing SUMO2/3-targeted ubiquitination and degradation

De-SUMOylation of FOXC2 by SENP3 promotes the epithelial-mesenchymal transition in gastric cancer cells

Toosendanin suppresses oncogenic phenotypes of human gastric carcinoma SGC-7901 cells partly via miR-200a-mediated downregulation of β-catenin pathway

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