Vasculogenic mimicry: Possible role of effector caspase-3, caspase-6 and caspase-7

Linder, Manuel; Tschernig, Thomas

doi:10.1016/j.aanat.2015.11.007

Cited by 17 publications

(8 citation statements)

References 43 publications

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“…Caspase-3 is a regulator of cell death ( 18 ). When caspase-3 is inhibited, apoptosis is prohibited, which contributes to tumorigenesis ( 19 ). A previous study demonstrated that caspase-3 and caspase-7 have synergistic effects in promoting apoptosis ( 20 ).…”

Section: Discussionmentioning

confidence: 99%

Naringin inhibits ovarian tumor growth by promoting apoptosis: An inï¿½vivo study

Cai

Hai-xia

et al. 2018

Oncol Lett

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The aim of the present study was to investigate the antitumor activities of naringin in ovarian cancer, and to assess the underlying mechanisms. Ovarian tumor cells were implanted into nude mice to produce ovarian tumors in vivo. The mice were divided into six groups: Control, low dose naringin [0.5 mg/kg, intraperitoneal (i.p.)], middle dose naringin (1 mg/kg, i.p.), high dose naringin (2 mg/kg, i.p.), positive control (cisplatin, 2 mg/kg, i.p.) and a combination of cisplatin and naringin (both 2 mg/kg). Following administration of naringin and/or cisplatin, the tumor size and weight were measured. Apoptosis of tumor cells was detected using a terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Apoptosis-associated gene expression was detected using reverse transcription-polymerase chain reaction and immunohistochemistry. In the range of 0.5–2 mg/kg, naringin dose-dependently inhibited tumor growth, as demonstrated by a decrease in tumor size and weight. Naringin promoted apoptosis of the ovarian tumor cells. Additionally, naringin reduced the expression of B-cell lymphoma (Bcl)-2, Bcl-extra large (Bcl-xL), cyclin D1, c-Myc and survivin, while it increased the expression of caspase-3 and caspase-7. The data demonstrated that naringin inhibited ovarian tumor growth in vivo. Its mechanisms may be associated with caspase-7-, caspase-3-, Bcl-2- and Bcl-xL-mediated apoptosis. Nevertheless, the clinical application of naringin in the treatment of ovarian cancer requires further study.

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Section: Discussionmentioning

confidence: 99%

Naringin inhibits ovarian tumor growth by promoting apoptosis: An inï¿½vivo study

Cai

Hai-xia

et al. 2018

Oncol Lett

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“…Mitochondrial dysfunction causes the release of cytochrome c into the cytosol. Subsequently, cytochrome c can combine with caspase-9 and apoptotic-protein activation factor-1 (Apaf-1) to start the apoptosis programme by forming the apoptosome, and the complex initiates further cascades that leading to apoptosis [ 41 ]. In addition, Bcl-2 family proteins regulate mitochondrial function, and the Bax/Bcl-2 ratio usually indicates the extent of apoptosis [ 42 ].…”

Section: Discussionmentioning

confidence: 99%

Resveratrol alleviates FFA and CCl4 induced apoptosis in HepG2 cells via restoring endoplasmic reticulum stress

Yang

et al. 2017

Oncotarget

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Cell apoptosis often induces inflammation and injury in the liver, with endoplasmic reticulum (ER) stress as the most possible reason. Resveratrol (RSV) has been shown to prevent hepatic steatosis and alleviate apoptosis, however, the exact mechanisms underlying the effects still need to be explored. Here we co-cultured HepG2 cells with free fatty acid (FFA) solution (oleic acid: palmitic acid = 2:1) and then exposed to a carbon tetrachloride (CCl4) solution to induce apoptosis. To evaluate the therapeutic effects, RSV (2.5 μM, 5 μM, 10 μM) was added to the cells. Results showed that HepG2 cells co-cultured with FFA exhibited lipid infiltration and were susceptible to apoptosis upon exposure to the CCl4 solution. The expression of molecules related to apoptosis (Caspases, Bcl-2/Bax) and ER stress (GRP78, IRE1, ATF6, PERK, et al.) was all significantly decreased upon RSV treatment. We further inhibited GRP78 by siRNA, results showed that the anti-apoptotic effect of RSV still maintained under GRP78 siRNA condition. Our data demonstrated that lipid accumulated HepG2 cells were susceptible to injury, and RSV could improve apoptosis in FFA and CCl4 stressed cells, which partially via restoring ER function.

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“…The free cytochrome c further binds to APAF-1 to form a cell death complex named apoptosome, and the later initiates cleavage on procaspase-9 to caspase-9. 44 – 46 Caspase-9 in turn activates the downstream effector caspases such as caspase-3 and the homolog, caspase-7 thus triggered the signaling cascade of apoptosis. 47 Interestingly, activation of APAF-1 lead to the downregulation of NAIP by −7.77 fold ( Table 1 ).…”

Section: Discussionmentioning

confidence: 99%

10<em>H</em>-3,6-Diazaphenothiazine induces G<sub>2</sub>/M phase cell cycle arrest and caspase-dependent apoptosis and inhibits cell invasion of A2780 ovarian carcinoma cells through the regulation of NF-κB and (BIRC6-XIAP) complexes

Zhang

Chen

Zhang³

et al. 2017

DDDT

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The asymptomatic properties and high treatment resistance of ovarian cancer result in poor treatment outcomes and high mortality rates. Although the fundamental chemotherapy provides promising anticancer activities, it is associated with severe side effects. The derivative of phenothiazine, namely, 10H-3,6-diazaphenothiazine (PTZ), was synthesized and reported with ideal anticancer effects in a previous paper. In this study, detailed anticancer properties of PTZ was examined on A2780 ovarian cancer cells by investigating the cytotoxicity profiles, mechanism of apoptosis, and cell invasion. Research outcomes revealed PTZ-induced dose-dependent inhibition on A2780 cancer cells (IC50 =0.62 µM), with significant less cytotoxicity toward HEK293 normal kidney cells and H9C2 normal heart cells. Generation of reactive oxygen species (ROS) and polarization of mitochondrial membrane potential (ΔΨm) suggests PTZ-induced cell death through oxidative damage. The RT2 Profiler PCR Array on apoptosis pathway demonstrated PTZ-induced apoptosis via intrinsic (mitochondria-dependent) and extrinsic (cell death receptor-dependent) pathway. Inhibition of NF-κB and subsequent inhibition of (BIRC6-XIAP) complex activities reduced the invasion rate of A2780 cancer cells penetrating through the Matrigel™ Invasion Chamber. Lastly, the cell cycle analysis hypothesizes that the compound is cytostatic and significantly arrests cell proliferation at G2/M phase. Hence, the exploration of the underlying anticancer mechanism of PTZ suggested its usage as promising chemotherapeutic agent.

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Vasculogenic mimicry: Possible role of effector caspase-3, caspase-6 and caspase-7

Cited by 17 publications

References 43 publications

Naringin inhibits ovarian tumor growth by promoting apoptosis: An inï¿½vivo study

Naringin inhibits ovarian tumor growth by promoting apoptosis: An inï¿½vivo study

Resveratrol alleviates FFA and CCl4 induced apoptosis in HepG2 cells via restoring endoplasmic reticulum stress

10<em>H</em>-3,6-Diazaphenothiazine induces G<sub>2</sub>/M phase cell cycle arrest and caspase-dependent apoptosis and inhibits cell invasion of A2780 ovarian carcinoma cells through the regulation of NF-κB and (BIRC6-XIAP) complexes

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Vasculogenic mimicry: Possible role of effector caspase-3, caspase-6 and caspase-7

Cited by 17 publications

References 43 publications

Naringin inhibits ovarian tumor growth by promoting apoptosis: An inï¿½vivo study

Naringin inhibits ovarian tumor growth by promoting apoptosis: An inï¿½vivo study

Resveratrol alleviates FFA and CCl4 induced apoptosis in HepG2 cells via restoring endoplasmic reticulum stress

10<em>H</em>-3,6-Diazaphenothiazine induces G<sub>2</sub>/M phase cell cycle arrest and caspase-dependent apoptosis and inhibits cell invasion of A2780 ovarian carcinoma cells through the regulation of NF-&kappa;B and (BIRC6-XIAP) complexes

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10<em>H</em>-3,6-Diazaphenothiazine induces G<sub>2</sub>/M phase cell cycle arrest and caspase-dependent apoptosis and inhibits cell invasion of A2780 ovarian carcinoma cells through the regulation of NF-κB and (BIRC6-XIAP) complexes