Bleomycin Suppresses the Proliferation and the Mobility of Human Gastric Cancer Cells Through the Smad Signaling Pathway

Liu, Jinfang; Nie, Xin; Shao, You-Cheng; Su, Wenhui; Hai-ying, MA; Xu, Xiaowu

doi:10.1159/000453192

Cited by 18 publications

(11 citation statements)

References 30 publications

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“…It was reported that TGF-β not only participates in tumorigenesis and development of cancer [42, 43], but also regulates the immune response as a key immune inhibitory cytokine [44], resulting in immune escape within the tumor microenvironment. Treg cells were also shown to play a significant role in the suppression of local antitumor immune responses through TGF-β secretion [45].…”

Section: Discussionmentioning

confidence: 99%

The Role of Tumoral FOXP3 on Cell Proliferation, Migration, and Invasion in Gastric Cancer

Zhang

et al. 2017

Cell Physiol Biochem

3,265

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Background/Aims: There is little published data on the role of FOXP3 in gastric cancer. Methods: FOXP3 expression and localization in gastric cancer tissues and cells were examined by immunohistochemistry, RT-PCR, flow cytometry, western blot, and laser confocal microscopy. CCK8, plate clone, wound healing, and transwell insert assays were performed for gastric cancer cells. Potential molecules and signaling pathways were screened using high-throughput transcriptome sequencing. Results: FOXP3 expression in gastric cancer tissues was higher than that in para-carcinoma tissues. It was restricted to the cytoplasm of para-carcinoma tissues, but was observed in the cytoplasm or/and nuclei of gastric cancer tissues. FOXP3 expression was positively correlated with pathological grading, and was detected in gastric cancer and GES-1 cells, where it was expressed in the cytoplasm alone, or in both the cytoplasm and the nucleus. FOXP3 overexpression promoted cell proliferation, migration, and invasion, while FOXP3 knockdown suppressed these effects. Furthermore, RT-PCR and ELISA confirmed that FOXP3 upregulation resulted in increased TGF-β expression and secretion in gastric cancer cells. Conclusion: FOXP3 expression was associated with degree of gastric cancer differentiation. In addition, upregulated and ectopic tumoral FOXP3 can promote gastric cancer proliferation, migration, and invasion, partly through the TGF-β pathway.

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Section: Discussionmentioning

confidence: 99%

The Role of Tumoral FOXP3 on Cell Proliferation, Migration, and Invasion in Gastric Cancer

Zhang

et al. 2017

Cell Physiol Biochem

3,265

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“…The CCK-8 method (Dojindo, Kumamoto, Japan) was used to detect cell proliferation ability [24, 25]. Second-generation EPCs were cultured in a flat-bottomed 96-well plate.…”

Section: Methodsmentioning

confidence: 99%

Asymmetric Dimethylarginine Induced Apoptosis and Dysfunction of Endothelial Progenitor Cells: Role of Endoplasmic Reticulum Stress Pathway

Zhou

Lin

et al. 2017

BioMed Research International

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Asymmetric dimethylarginine (ADMA), an inhibitor of nitric oxide synthase, is a novel risk factor of cardiovascular disease. Endothelial progenitor cells (EPCs) bear typical endothelial characteristics and are thought to contribute to neovascularization by providing new endothelial cells (ECs) after arterial injury. Many studies have shown that ADMA can induce EPC apoptosis and dysfunction, but the underlying mechanism is not well understood. EPCs from umbilical cord blood were cultured in EGM-2 medium with particular growth factors and supplemented with 10% fetal bovine serum. The cells were treated with different concentrations of ADMA (5, 10, and 50 μmol/L). Endoplasmic reticulum (ER) stress marker levels were examined by western blot analysis. After 24-hour incubation, ADMA induced apoptosis of EPCs and significantly decreased the proliferation, migration, and vasculogenesis capacity of EPCs. We also found that ADMA treatment activated phosphorylated protein kinase RNA-activated-like ER kinase (PERK), a stress sensor protein in the endoplasmic reticulum (ER). The activated PERK induced 78 kDa glucose-regulated protein (GRP-78) and C/EBP homologous protein (CHOP) expression. Additionally, the inhibition of the ER stress pathway by Salubrinal (a specific ER stress inhibitor) can attenuate ADMA-induced apoptosis of EPCs. Overall, these observations indicate that ADMA may induce the apoptosis and dysfunction of EPCs through the ER stress pathway.

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“…The Smad signaling pathway is a pivotal pathway in regulating a range of cellular functions in cancer cells, including proliferation, mobility, and apoptosis. 11 Central mediators of the Smad pathways are Smad2 and Smad3. They are phosphorylated and activated through the formation of the phosphorylation of Smad2 (ser465/467) and Smad3 (ser423/425).…”

Section: Introductionmentioning

confidence: 99%

“…They are phosphorylated and activated through the formation of the phosphorylation of Smad2 (ser465/467) and Smad3 (ser423/425). 11 P-Smad2 and P-Smad3 formed complexes with Smad4 that accumulate in the nucleus and regulate the progression of cancer cells. 11 This is the first report to show the influence of ING5 on the Smad signaling pathway in OS cells.…”

Section: Introductionmentioning

confidence: 99%

ING5 is a Potential Target for Osteosarcoma Therapy

Zhang

Xie

et al. 2018

Technol Cancer Res Treat

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Osteosarcoma is one of the most common primary malignant bone tumors. The inhibitor of growth family of protein 5 has been identified as a tumor suppressor in many cancers. In this study, we confirmed the downregulation of the both inhibitor of growth family of protein 5 and messenger RNA levels in cancer tissues using Western blot and real-time polymerase chain reaction. In order to find the antitumor roles of inhibitor of growth family of protein 5, osteosarcoma cells, HOS, and MG63 were transfected with the plasmid pCDNA-3.1-inhibitor of growth family of protein 5. Overexpression of Inhibitor of growth family of protein 5 could induce apoptosis and inhibit cell proliferation in osteosarcoma cells. Furthermore, Western blot analysis showed that p-Smad2, p-Smad3, and Smad4 were increased in inhibitor of growth family of protein 5-expressing osteosarcoma cells. Our results indicated that overexpression of inhibitor of growth family of protein 5 in osteosarcoma cells induces apoptosis by activating the Smad pathway, thus proposing a promising role for inhibitor of growth family of protein 5 in treatment of patients with osteosarcoma.

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Bleomycin Suppresses the Proliferation and the Mobility of Human Gastric Cancer Cells Through the Smad Signaling Pathway

Cited by 18 publications

References 30 publications

The Role of Tumoral FOXP3 on Cell Proliferation, Migration, and Invasion in Gastric Cancer

The Role of Tumoral FOXP3 on Cell Proliferation, Migration, and Invasion in Gastric Cancer

Asymmetric Dimethylarginine Induced Apoptosis and Dysfunction of Endothelial Progenitor Cells: Role of Endoplasmic Reticulum Stress Pathway

ING5 is a Potential Target for Osteosarcoma Therapy

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