TRAIL-induced apoptosis of human melanoma cells involves activation of caspase-4

Mao, Zhi Gang; Jiang, Chen Chen; Yang, Fan; Thorne, Rick F.; Hersey, Peter; Zhang, Xu Dong

doi:10.1007/s10495-010-0513-9

Cited by 26 publications

(19 citation statements)

References 40 publications

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“…Increased expression of MMPs was closely correlated with tumor invasion and metastasis [33−36]. CASP4 was upregulated after HIC-1 activation, which is an apoptosis-related cysteine peptidase [37], [38]. BIK, which is a BCL2-interacting killer related to apoptotic induction, was also upregulated [39−42].…”

Section: Discussionmentioning

confidence: 99%

Small Activating RNA Restores the Activity of the Tumor Suppressor HIC-1 on Breast Cancer

Zhao

Pan

et al. 2014

PLoS ONE

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HIC-1 is a gene that is hypermethylated in cancer, and commonly downregulated in human breast cancer. However, the precise mechanisms and molecular pathways regulated by HIC-1 remain unclear. We assessed HIC-1 expression on a tissue microarray containing 80 cases of breast cancer. We also analyzed its biological function by restoring HIC-1 expression using 5-aza-2′ deoxycytidine (5-CdR) and small-activating RNAs for the reversal of HIC-1 tumor suppressive effects on MCF-7 and MDA-MB-231 cell lines. An Agilent Q44h global expressing microarray was probed after restoring the expression of HIC-1. Data demonstrated that HIC-1 expression was reduced significantly in breast cancer tissues. HIC-1 immunohistochemistry resulted in mean staining scores in cancer tissue and normal ductal epithelia of 3.54 and 8.2, respectively (p<0.01). 5-CdR partially reversed HIC-1 expression, and modulated cell growth and apoptosis. dsHIC1-2998, an saRNA, showed activating efficacy in breast cancer cells. A group of differentially expressed genes were characterized by cDNA microarray. Upon saRNA treatment, genes upregulated included those involved in immune activation, cell cycle interference, the induction of apoptosis, anti-metastasis, and cell differentiation. Downregulated genes included oncogenes and those that play roles in cell invasion, cell growth, and cell division. Our findings may provide valuable resources not only for gene functional studies, but also for potential clinical applications to develop novel drug targets.

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Section: Discussionmentioning

confidence: 99%

Small Activating RNA Restores the Activity of the Tumor Suppressor HIC-1 on Breast Cancer

Zhao

Pan

et al. 2014

PLoS ONE

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“…Caspase-4 was recently shown to be involved in TRAIL-induced apoptosis of human melanoma cells. However, inhibition of caspase-4 partially, but not completely, blocked apoptosis (39), suggesting that its role is limited. Since caspase-4 has been shown to be activated later than caspase-8, caspase-9 and caspase-3 (39), it is possible that caspase-4 and caspase-12 may play roles in different processes/stages in ER stress-induced apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…However, inhibition of caspase-4 partially, but not completely, blocked apoptosis (39), suggesting that its role is limited. Since caspase-4 has been shown to be activated later than caspase-8, caspase-9 and caspase-3 (39), it is possible that caspase-4 and caspase-12 may play roles in different processes/stages in ER stress-induced apoptosis. Our preliminary attempt to establish caspase-12 gene knockdown cells was hampered by considerable cell death in the resting state.…”

Section: Discussionmentioning

confidence: 99%

Depolarization potentiates TRAIL-induced apoptosis in human melanoma cells: Role for ATP-sensitive K+ channels and endoplasmic reticulum stress

Suzuki¹,

Inoue²,

Murai³

et al. 2012

International Journal of Oncology

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Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is promising for cancer treatment owing to its selective cytotoxicity against malignant cells. However, some cancer cell types, including malignant melanoma cells, are resistant to TRAIL-induced apoptosis. Therefore, drugs that can amplify TRAIL cytotoxicity are urgently required. Depolarization of the plasma membrane potential is associated with apoptosis induced by a variety of death-inducing agents but its role in apoptosis remains a matter of debate. We found that TRAIL treatment resulted in robust depolarization in human melanoma cells with a considerable lag (2–4 h). Moreover, membrane-depolarizing agents, including K+ and ATP-sensitive K+ (KATP) channel inhibitors glibenclamide and U37883A enhanced TRAIL-induced apoptosis. On the contrary, inhibitors of calcium- and voltage-dependent K+ channels and mitochondrial KATP channels had no such effects. Melanocytes were insensitive to TRAIL-induced depolarization and apoptosis as well as to the sensitization by membrane-depolarizing agents despite their substantial surface expression of death receptors. TRAIL induced robust activation of X-box-binding protein-1 and caspase-12, both of which were enhanced by the K+ and KATP channel inhibitors, but not by other K+ channel inhibitors. Finally, caspase-12-selective inhibitor completely abolished the amplification of apoptosis. These findings suggest that depolarization promotes endoplasmic reticulum stress-mediated death pathway, thereby amplifying TRAIL cytotoxicity. Thus, membrane-depolarizing agents such as KATP channel inhibitors may have therapeutic potential in the treatment of TRAIL-resistant cancer cells without impairing tumor-selectivity.

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“…In particular, caspase-4, located on the outer membrane of the endoplasmic reticulum, has been found to be involved in stress-related apoptosis of the endoplasmic reticulum (16–18). In addition, some studies also indicated that caspase-4 plays an important role in the TRAIL-induced apoptosis (19,20). …”

Section: Discussionmentioning

confidence: 99%

Correlation between NF-κB signal pathway-mediated caspase-4 activation and Kawasaki disease

Tian

Niu

2017

Experimental and Therapeutic Medicine

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The aim of the study was to investigate the role and mechanisms of action of nuclear factor-κB (NF-κB)-mediated caspase-4 activation in the induction of inflammatory cytokines during Kawasaki disease (KD) and coronary artery endothelial cell injury. Peripheral blood mononuclear cells (PBMCs) were isolated from KD patients and healthy controls and cultured. Double antibody sandwich enzyme-linked immunosorbent assay (ELISA) was applied to detect tumor necrosis factor (TNF)-α levels in activated PBMC-conditioned culture media. To establish a culture model for human coronary artery endothelial cells (HCAECs), we employed KD patient-origin PBMC culture-conditioned media to induce HCAEC transformation and detected the nuclear activation of NF-κB p65 and intracellular caspase-4 protein concentrations using western blot analysis. We also investigated the nuclear transfer of NF-κB p65 using immunofluorescence, as well as HCAEC interleukin (IL)-6 and IL-1β secretion using ELISA. Finally, we investigated HCAEC apoptosis using using Annexin V/PI double staining. After PBMCs were stimulated in vitro, TNF-α secretion was significantly higher in the KD group versus controls (P<0.01). HCAEC cells treated with supernatant conditioned by cells from KD patients showed a significant elevation of NF-κB p65 and caspase-4 protein expression versus HCAEC cells treated with supernatant conditioned by control cells (P<0.01). Similarly, IL-6 and IL-1β secretion, as well as apoptotic rate, were significantly elevated (P<0.01). SN50, an NF-κB inhibitor, significantly attenuated caspase-4 expression, secretion of IL-6, IL-1β, and TNF-α, as well as HCAEC apoptosis in cells treated with KD patient PBMC-conditioned media. NF-κB can induce the generation of various inflammatory factors including IL-6 and IL-1β, mediate the expression of caspase-4 in HCAEC cells, and affect apoptosis and injury of HCAEC cells. Therefore, the expression of caspase-4, mediated by NF-κB signal pathway, plays a critical role in KD.

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TRAIL-induced apoptosis of human melanoma cells involves activation of caspase-4

Cited by 26 publications

References 40 publications

Small Activating RNA Restores the Activity of the Tumor Suppressor HIC-1 on Breast Cancer

Small Activating RNA Restores the Activity of the Tumor Suppressor HIC-1 on Breast Cancer

Depolarization potentiates TRAIL-induced apoptosis in human melanoma cells: Role for ATP-sensitive K+ channels and endoplasmic reticulum stress

Correlation between NF-κB signal pathway-mediated caspase-4 activation and Kawasaki disease

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