Bcl‐2 and caspase‐8 related anoikis resistance in human osteosarcoma MG‐63 cells

Lin, Dong; Feng, Jie; Chen, Weishan

doi:10.1016/j.cellbi.2008.07.002

Cited by 13 publications

(10 citation statements)

References 26 publications

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“…3). In osteosarcoma cells, Lin et al recently reported an upregulation of Bcl-2 and increased resistance to anoikis [26], supporting our finding and the positive regulatory role of Bcl-2 in anoikis resistance. The role of Cav-1 in anoikis resistance and metastasis has been reported but remains controversial.…”

Section: Discussionsupporting

confidence: 91%

“…Bcl-2 and Cav-1 attenuate detachment-induced cell death in H460 cells Bcl-2 and Cav-1 have been implicated in anoikis resistance of various cancer cell types [17,26,[34][35][36]. To investigate whether Bcl-2 and Cav-1 could attenuate anoikis in H460 cells, the cells were stably transfected with Bcl-2 or Cav-1 plasmid and analyzed for the respective protein expression by Western blotting.…”

Section: Curcumin Sensitizes Lung Carcinoma H460 Cells To Detachment-mentioning

confidence: 99%

“…Such dysregulation disrupts mitochondrial function, causing the release of cytochrome c from the mitochondrial intermembrane space and subsequent activation of caspase cascades [24,25]. An upregulation of Bcl-2 has been shown to suppress anoikis of cancer cells [18,26]. The expression of Bcl-2 is tightly regulated by different mechanisms, including transcription, heterodimerization, posttranslational modifications and degradation.…”

Section: Introductionmentioning

confidence: 99%

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Curcumin sensitizes non-small cell lung cancer cell anoikis through reactive oxygen species-mediated Bcl-2 downregulation

et al. 2010

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Anoikis, an apoptosis triggered by loss of cell anchorage, has been shown to be a principal mechanism of inhibition of tumor metastasis. Recently, anti-apoptotic Bcl-2 and Cav-1 proteins have been demonstrated to be highly associated with tumor metastasis and apoptosis resistance. Curcumin, a major active component of turmeric, Curcuma longa, has been shown to inhibit neoplastic evolution and tumor progression; however, the underlying mechanisms are unclear. In this study, we investigated the effect of curcumin on cell anoikis as a possible mechanism of anti-tumorigenic action of curcumin, and evaluated the potential role of Bcl-2 and Cav-1 in this process. Our results showed that ectopic expression of either Bcl-2 or Cav-1 induced anoikis resistance of lung carcinoma H460 cells. Curcumin downregulated Bcl-2 protein during anoikis and sensitized the cells to detachment-induced apoptosis, whereas it had no significant effect on Cav-1 protein expression. Bcl-2 down-regulation as well as anoikis enhancement by curcumin were inhibited by superoxide anion scavenger, Mn(III)tetrakis(4-benzoic acid) porphyrin chloride, but were unaffected by other ROS scavengers including catalase and deferoxamine, suggesting that superoxide anion is a key player in the downregulation of Bcl-2 by curcumin. Furthermore, we provided evidence that curcumin decreased Bcl-2 level through ubiquitin-proteasomal degradation which sensitized cells to detachment-induced apoptosis. These findings indicate a novel pathway for curcumin regulation of Bcl-2 and provide a key mechanism of anoikis regulation that may be exploited for metastatic cancer treatment.

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Section: Discussionsupporting

confidence: 91%

Section: Curcumin Sensitizes Lung Carcinoma H460 Cells To Detachment-mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Curcumin sensitizes non-small cell lung cancer cell anoikis through reactive oxygen species-mediated Bcl-2 downregulation

et al. 2010

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“…Several studies have demonstrated that malignant cells acquire anoikis resistance through an upregulation of antiapoptotic proteins such as c-FLIP 36,37 and Bcl-2 38,39 (Fig. 5).…”

Section: Ivb No and Apoptosis Regulatory Proteinsmentioning

confidence: 99%

Nitrosothiol Signaling in Anoikis Resistance and Cancer Metastasis

Luanpitpong

Iyer

Azad

et al. 2012

Forum Immun Dis Ther

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Nitric oxide (NO) has been widely recognized as an important cell-signaling molecule that regulates various physiological and pathological processes. S-nitrosylation, or covalent attachment of NO to protein sulfhydryl groups, is a key mechanism by which NO regulates protein functions and cellular processes. In this article we discuss the various roles of NO and protein nitrosylation in cancer development, with a focus on cell invasion and anoikis resistance, both of which are key determinants of cancer metastasis. We specially address some of the mechanisms by which NO-mediated S-nitrosylation modulates substrates that have putative effects on key steps of metastasis. We propose that nitrosothiol signaling is a key regulatory mechanism common to several pathways involved in cancer progression and metastasis, and identifying such a mechanism will improve our understanding of the disease process and aid in the development of novel anticancer therapeutics.

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“…Our previous work has shown that human MG-63 osteosarcoma cells form large and dense aggregates in suspension, without significant apoptosis-a feature of anoikis evasion (Lin et al, 2008;Lin, 2012). Following suspension, the osteosarcoma cells adhere to each other and form clumps, which simulates the environment of cell-matrix adhesion, and allows the osteosarcoma cells to avoid anoikis.…”

Section: Correlation Between E-cadherin-regulated Cell Adhesion and Hmentioning

confidence: 99%

Correlation between E-Cadherin-Regulated Cell Adhesion and Human Osteosarcoma MG-63 Cell Anoikis

Lin

Cai²,

Ding³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Purpose: The aim of this study was to investigate the relationship between cell adhesion and anoikis evasion among human osteosarcoma cells (MG-63), and to further study the molecular mechanisms. Materials and Methods: Human osteosarcoma cells (MG-63) were assessed for apoptosis, and caspase-3, E-cadherin and β-catenin expression in EDTA and control non-EDTA groups. Results: MG-63 cells were predominantly aggregated when in suspension, and the suspended cells were more dispersed in the EDTA group. Following culture in suspension for 24 h, 48 h, or 72 h, the rates of apoptosis were 34.88%±3.64%, 59.3%±7.22% and 78.5%±5.21% in the experimental group and 7.34%±2.13%, 14.7%±3.69%, and 21.4%±3.60% in the control group, respectively. Caspase-3 expression progressively increased and E-cadherin and β-catenin were decreased in the experimental group, whereas there was no change in the control group. Conclusions: MG-63 cells could avoid anoikis through cell adhesion, and E-cadherin might play a role in this process.

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Bcl‐2 and caspase‐8 related anoikis resistance in human osteosarcoma MG‐63 cells

Cited by 13 publications

References 26 publications

Curcumin sensitizes non-small cell lung cancer cell anoikis through reactive oxygen species-mediated Bcl-2 downregulation

Curcumin sensitizes non-small cell lung cancer cell anoikis through reactive oxygen species-mediated Bcl-2 downregulation

Nitrosothiol Signaling in Anoikis Resistance and Cancer Metastasis

Correlation between E-Cadherin-Regulated Cell Adhesion and Human Osteosarcoma MG-63 Cell Anoikis

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