Dying to hold you

Doukoumetzidis, Kimon; Hengartner, Michael O.

doi:10.1038/451530a

Cited by 7 publications

(4 citation statements)

References 9 publications

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“…ZHAOFENG CHEN 1,2 , MIN LIU 1,2 , XIAOJUN LIU 1,2 , SHANSHAN HUANG 3 , LINLIN LI 1 , BO SONG 1 , HAILONG LI 1 , QIAN REN 1,2 , ZENAN HU 1 , YONGNING ZHOU 1,2 and LIANG QIAO 4 tion of apoptosis and the enhancement of neovascularization. Thus, COX-2 significantly contributes to carcinogenesis (5,6).…”

Section: Cox-2 Regulates E-cadherin Expression Through the Nf-κb/snaimentioning

confidence: 99%

“…E-cadherin is one of the most important adhesion molecules and is essential for the maintenance of intact cellular functionality. The inhibition of tumor invasion and metastasis are among the most important biological functions of E-cadherin, as its abnormal expression and function have been observed in several epithelium-derived cancers including gastric cancer (2)(3)(4).…”

Section: Introductionmentioning

confidence: 99%

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COX-2 regulates E-cadherin expression through the NF-κB/Snail signaling pathway in gastric cancer

Chen

Liu

et al. 2013

International Journal of Molecular Medicine

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Cyclooxygenase-2 (COX-2) participates in cancer invasion and metastasis by decreasing the expression of E-cadherin. However, the molecular mechanisms through which COX-2 regulates E-cadherin expression and function have not yet been fully elucidated. The aim of this study was to investigate the possible molecular mechanisms through which COX-2 regulates E-cadherin expression in gastric cancer. The mRNA and protein expression of COX-2, nuclear factor-κB (NF-κB), Snail and E-cadherin was detected in gastric cancer cells by quantitative PCR and western blot analysis, respectively. The expression of these genes was also detected in healthy gastric mucosa and gastric cancer tissues by immunohistochemistry. We detected various levels of COX-2, nuclear factor-κB (NF-κB), Snail and E-cadherin expression in the normal gastric mucosa and cancer tissues; however, the expression patterns differed: the increased expression of COX-2, NF-κB and Snail was observed in the gastric cancer tissues, whereas there was a considerable reduction in E-cadherin expression in the cancer tissues compared to the normal gastric mucosa. The expression patterns of COX-2, NF-κB and Snail were similar. The increased expression of COX-2 in the gastric cancer tissues closely correlated with the increased expression of NF-κB and Snail, but inversely correlated with the expression of E-cadherin. Treatment of the SGC7901 cells (which express high levels of COX-2) with celecoxib, a COX-2 inhibitor, not only led to a marked dose- and time-dependent decrease in the expression of COX-2, NF-κB and Snail, but also led to a significant increase in the expression of E-cadherin, and this was associated with a reduction in cell invasion. By contrast, the same treatment did not alter the expression of these genes in another gastric cancer cell line, MGC803 (which barely expresses COX-2). These data suggest that COX-2 regulates the expression of E-cadherin through the NF-κB and Snail signaling pathway in gastric cancer.

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Section: Cox-2 Regulates E-cadherin Expression Through the Nf-κb/snaimentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

COX-2 regulates E-cadherin expression through the NF-κB/Snail signaling pathway in gastric cancer

Chen

Liu

et al. 2013

International Journal of Molecular Medicine

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“…9, 11, 40, 44, 45 Their biological mechanisms 3, 6, 34, 35 and pathogenic roles are starting to emerge. 7, 10, 27 Although some investigators questioned the cell-in-cell processes as an in vitro phenomenon, almost all observations of cell-in-cell structures were reported from clinical biopsy specimens.…”

Section: Cell-in-cell Structure Formation: An In Situ Activity or A Hmentioning

confidence: 99%

Modeling cell-in-cell structure into its biological significance

Wang

Wang³

et al. 2013

Cell Death Dis

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Although cell-in-cell structure was noted 100 years ago, the molecular mechanisms of ‘entering' and the destination of cell-in-cell remain largely unclear. It takes place among the same type of cells (homotypic cell-in-cell) or different types of cells (heterotypic cell-in-cell). Cell-in-cell formation affects both effector cells and their host cells in multiple aspects, while cell-in-cell death is under more intensive investigation. Given that cell-in-cell has an important role in maintaining homeostasis, aberrant cell-in-cell process contributes to the etiopathology in humans. Indeed, cell-in-cell is observed in many pathological processes of human diseases. In this review, we intend to discuss the biological models of cell-in-cell structures under physiological and pathological status.

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“…Previous studies demonstrated that entosis depends on E-cadherin, the cell adhesion protein transducing a contractile force between the actomyosin cytoskeleton and plasma membrane 15 . The actomyosin complex of the invading cell plays an important role during penetration 4 , 5 , 16 , 17 . In addition, the microtubule-based cytoskeleton participates in entosis by regulating cell rigidity 18 .…”

Section: Introductionmentioning

confidence: 99%

Consecutive entosis stages in human substrate-dependent cultured cells

Garanina

Kisurina-Evgenieva

Ерохина

et al. 2017

Sci Rep

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Entosis, or cell death by invading another cell, is typical for tumor epithelial cells. The formation of cell-in-cell structures is extensively studied in suspension cultures, but remains poorly understood in substrate-dependent cells. Here, we used electron, confocal and time-lapse microscopy in combination with pharmacological inhibition of intracellular components to study the kinetics of entosis using two human substrate-dependent tumor cultures, A431 and MCF7. In total, we identified and characterized five consecutive stages of entosis, which were common for both examined cell lines. We further demonstrated that actin filaments in the entotic as well as invading cells were crucial for entosis. Microtubules and the Golgi apparatus of entotic cells provided membrane expansion required for internalization of the invading cell. Depolymerization of microfilaments and microtubules, and disintegration of the Golgi complex inhibited entosis. We confirmed the presence of adhesive junctions and discovered the formation of desmosomes between the invading and entotic cells. The internalized cell was shown to be degraded due to the lysosomal activation in both cells whereas the disintegration of the Golgi apparatus did not affect the process. Thus, in the substrate-dependent cultures, entosis requires microfilaments, microtubules and the Golgi complex for cell invasion, but not for internalized cell degradation.

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Dying to hold you

Cited by 7 publications

References 9 publications

COX-2 regulates E-cadherin expression through the NF-κB/Snail signaling pathway in gastric cancer

COX-2 regulates E-cadherin expression through the NF-κB/Snail signaling pathway in gastric cancer

Modeling cell-in-cell structure into its biological significance

Consecutive entosis stages in human substrate-dependent cultured cells

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