Mitochondria-Dependent Apoptosis Induced by Nanoscale Hydroxyapatite in Human Gastric Cancer SGC-7901 Cells

Chen, Xiaojuan; Deng, Changsheng; Tang, Shengli; Zhang, Ming

doi:10.1248/bpb.30.128

Cited by 87 publications

(79 citation statements)

References 24 publications

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“…For example, hydroxyapatite-containing "atherosclerotic gruel"-induced apoptosis in macrophages, 25 and calcium phosphate nanocrystals have been reported to induce apoptosis in cancer cells. 26 In synovial fibroblasts, proliferation is enhanced in the presence of calcium phosphate crystals, 7 Because of the heterogeneous nature of VSMCs, it is possible that one population of VSMCs within each isolate has different calcium handling mechanisms, phagocytosis kinetics, or susceptibility to cell death. Experiments using bafilomycin A1 showed that inhibition of lysosomal proton pump activity reduced the magnitude of [Ca 2ϩ ] i rises and inhibited cell death induced by BCP.…”

Section: Discussionmentioning

confidence: 99%

Calcium Phosphate Crystals Induce Cell Death in Human Vascular Smooth Muscle Cells

Ewence

Bootman

Roderick

et al. 2008

Circulation Research

293

246

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Abstract-Vascular calcification is associated with an increased risk of myocardial infarction; however, the mechanisms linking these 2 processes are unknown. Studies in macrophages have suggested that calcium phosphate crystals induce the release of proinflammatory cytokines; however, no studies have been performed on the effects of calcium phosphate crystals on vascular smooth muscle cell function. In the present study, we found that calcium phosphate crystals induced cell death in human aortic vascular smooth muscle cells with their potency depending on their size and composition. Calcium phosphate crystals of approximately 1 m or less in diameter caused rapid rises in intracellular calcium concentration, an effect that was inhibited by the lysosomal proton pump inhibitor, bafilomycin A1. Bafilomycin A1 also blocked vascular smooth muscle cell death suggesting that crystal dissolution in lysosomes leads to an increase in intracellular calcium levels and subsequent cell death. These studies give novel insights into the bioactivity of calcified deposits and suggest that small calcium phosphate crystals could destabilize atherosclerotic plaques by initiating inflammation and by causing vascular smooth muscle cell death. (Circ Res. 2008;103:e28-e34.)

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Section: Discussionmentioning

confidence: 99%

Calcium Phosphate Crystals Induce Cell Death in Human Vascular Smooth Muscle Cells

Ewence

Bootman

Roderick

et al. 2008

Circulation Research

293

246

View full text Add to dashboard Cite

show abstract

“…Human gastric cancer SGC-7901 cells, a common cell line, were used to study antigastric cancer of drugs in vitro (Chen et al, 2007;Ji et al, 2011;Li & Xu, 2003), especially anthraquinones, such as rhein (Li et al, 2012) and emodin (Cai et al, 2008;Sun & Bu, 2012). Metabolism and growth rate of cells could be out of control due to the activation of proto-oncogene of normal cells.…”

Section: Discussionmentioning

confidence: 99%

Anticancer effect of 2,7-dihydroxy-3-methylanthraquinone on human gastric cancer SGC-7901 cellsin vitroandin vivo

Zhu

Zheng

Zhang

et al. 2015

Pharmaceutical Biology

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Objective: The objective of this study is to study the anticancer effect and mechanism of DDMN on SGC-7901 cells. Materials and methods: The MTT assay was used to determine the effect of DDMN on cell viability of SGC-7901 cells, and the cytotoxic effect was evaluated by the IC 50 value. After treatment with different doses of DDMN (10, 20, and 40 mM) for 48 h, flow cytometry was used to investigate the apoptosis of SGC-7901 cells induced by DDMN. Further, western blotting was performed to study anticancer mechanism by assaying apoptosis-related proteins containing Mcl-1, Bcl-xl, Bcl-2, Bax, Bak, Bad, cytochrome c, caspase-3, and caspase-9. Finally, xenograft assay was used to further evaluate the effect of DDMN on SGC-7901 cells by determining body weight of nude mice, tumor volumes, and apoptosis-related proteins. Results: These results suggest that DDMN can significantly inhibit (IC 50 value ¼ 20.92 mM) the proliferation of SGC-7901 cells and induce apoptosis of SGC-7901 cells demonstrated by flow cytometry analysis. Additionally, the results of western blotting indicated that DDMN can suppress the expression of anti-apoptotic proteins Bcl-xl and Bcl-2, increase the expression of pro-apoptotic proteins Bax, Bad (40 mM), caspase-3 and caspase-9, and evidently promote the release of cytochrome c from the mitochondria to the cytoplasm. The xenograft assay further confirmed that DDMN had significant anticancer effects on SGC-7901 cells. Conclusion: DDMN had significant anticancer effect on SGC-7901 cells in vitro and in vivo related to mitochondria-mediated apoptosis.

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“…Currently, GC relies on surgery combined with chemotherapy and adjuvant chemoradiotherapy for its clinical treatment, which is somewhat effective in prolonging patients’ overall survival and relapse-free survival but failed to inhibit GC recurrence and metastasis [5, 6]. Furthermore, in spite of the advances in early diagnosis and treatment modalities, the side effects of chemotherapy and frequent recurrence remain tricky problems in its treatment, thus fueling a great need for identification of new and effective anti-cancer agents for reducing the mortality [7]. It has been revealed that certain genes such as vitamin E succinate (VES) can block cell cycle, arrest DNA synthesis and induce apoptosis in human GC SGC-7901 cells, therefore inhibiting cell growth [8].…”

Section: Introductionmentioning

confidence: 99%

SUMO-1 Gene Silencing Inhibits Proliferation and Promotes Apoptosis of Human Gastric Cancer SGC-7901 Cells

Jin

Shen

Chen

et al. 2017

Cell Physiol Biochem

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Background: It has been reported that blocking small ubiquitin-like modifier (SUMO) conjugation by silencing SUMO gene remarkably decreased tumor growth in vivo. However, few studies have examined the relationship between SUMO gene silencing and gastric cancer (GC). The study aims to explore the effects of SUMO-1 gene silencing on GC cell proliferation and apoptosis. Methods: GC cells were cultured and divided into 5 groups: the blank group (without any transfection or treatment), the empty vector group (transfected with empty vector), the shRNA-SUMO-1-1 group (transfected with shRNA-SUMO-1-1 plasmid), the shRNA-SUMO-1-2 group (transfected with shRNA-SUMO-1-2 plasmid), and the shRNA-SUMO-1-3 group (transfected with shRNA-SUMO-1-3 plasmid). Cell Counting Kit-8 (CCK-8) assay was performed to examine cell proliferation. Annexin V/PI staining combined with flow cytometry were used to detect cell apoptosis. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were employed to measure the mRNA and protein expressions of SUMO-1, P53, Bcl-2 and c-myc, respectively. Results: SUMO-1 mRNA and protein expressions were decreased after transfecting with shRNA-SUMO-1. Compared with the blank group, the shRNA-SUMO-1-1 group presented a remarkable decreased proliferation of SGC-7901 cells. Significant increase in cell apoptosis rate was observed. Bcl-2, c-myc and P53 expressions were declined after transfecting with shRNA-SUMO plasmid. Conclusion: Our study provided evidence that SUMO-1 gene silencing could decrease proliferation and promote apoptosis in GC cells.

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Mitochondria-Dependent Apoptosis Induced by Nanoscale Hydroxyapatite in Human Gastric Cancer SGC-7901 Cells

Cited by 87 publications

References 24 publications

Calcium Phosphate Crystals Induce Cell Death in Human Vascular Smooth Muscle Cells

Calcium Phosphate Crystals Induce Cell Death in Human Vascular Smooth Muscle Cells

Anticancer effect of 2,7-dihydroxy-3-methylanthraquinone on human gastric cancer SGC-7901 cellsin vitroandin vivo

SUMO-1 Gene Silencing Inhibits Proliferation and Promotes Apoptosis of Human Gastric Cancer SGC-7901 Cells

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