In addition, several studies have shown that apigenin-induced apoptosis involves both the intrinsic and extrinsic apoptotic pathways [, ].
The present study supports the hypothesis that apigenin-induced apoptosis involves the activation of both the intrinsic and extrinsic apoptotic pathways.
Then after, to investigate the apoptosis induction by apigenin, cells were exposed to either vehicle or apigenin (at the IC50 concentration) and incubated for 72 h.
Thus, in the present study, we investigated the modulation of the initiator caspase in the extrinsic or intrinsic pathway during apigenin-induced apoptosis.
Apigenin and silybinin significantly reduced cell number, with apigenin inducing apoptosis in PWR-1E, LNCaP, PC-3, and DU145 cells.
Focusing specifically on apigenin we assessed the ability of calpain, serine protease, caspase, estrogen receptor, and ceramide synthase inhibitors to block apigenin induced apoptosis.
The overexpression of Bcl-2 in LNCaP B10 cells reduced the apoptotic effects of apigenin.
The PC-3 and DU145 cells were less susceptible to apigenin induced apoptosis then LNCaP and PWR-1E cells.
In addition, suppression of DR5 expression with siRNA efficiently reduced luteolin-induced caspase activation and apoptosis.
In this report, we reveal a novel mechanism by which luteolin-induced apoptosis occurs, and show for the first time that the apoptosis by luteolin is mediated through death receptor 5 (DR5) upregulation.
These results suggest that DR5 induced by luteolin plays a role in luteolin-induced apoptosis, and raises the possibility that treatment with luteolin might be promising as a new therapy against cancer.
Apigenin increased caspase-3 activity and PARP cleavage, and Z-VAD-FMK, a broad-spectrum caspase-3 inhibitor, rescued NUB-7 cells from apigenin-mediated apoptosis indicating that apigenin induced apoptosis in acaspase-dependent manner.
Apigenin inhibited colony-forming ability and survival, and induced apoptosis of NUB-7 and LAN-5 cells.
Apigenin is thus a candidate therapeutic for neuroblastoma that likely acts by regulating a p53-Bax-caspase-3 apoptotic pathway.
We investigated the ability of apigenin, a nonmutagenic dietary flavonoid that has been shown to have antitumor effects in various tumor cell lines, to inhibit growth and induce apoptosis of the human neuroblastoma cell lines NUB-7, LAN-5, and SK-N-BE(2).
Treatment with the caspase inhibitors Z-VAD-FMK and DEVD-CHO partially rescued these cells from apigenin-induced apoptosis.
These results indicate that apigenin-induced apoptosis in 22Rv1 cells is initiated by a ROS-dependent disruption of the mitochondrial membrane potential through transcriptional-dependent and -independent p53 pathways.
In vivo, apigenin administration demonstrated p53-mediated induction of apoptosis in 22Rv1 tumors.
This suggests that apoptosis induced by BE is independent of the production of ROS in HL-60 cells.
This suggests that activation of PKC and JNKs participate in TPA's prevention of BE-induced apoptosis via suppressing mitochondrial dysfunction in HL-60 cells.
The ROS-scavenging activity of BE was identified by the anti-DPPH radical, DCHF-DA, and in vitro plasmid digestion assay, and none of chemical antioxidants including allpurinol (ALL), N-acetyl-cystein (NAC), and diphenylene iodonium (DPI) affected BE-induced apoptosis in HL-60 cells.
TPA addition induces the phosphorylation of JNKs and ERKs, but not p38, protein in HL-60 cells, and incubation of HL-60 cells with JNKs inhibitor SP600125, but not ERKs inhibitor, PD98059 or the p38 inhibitor SB203580, suppressed the protective effect of TPA against BE-induced apoptotic events including DNA ladders, apoptotic bodies, caspase 3 and D4-GDI protein cleavage in according with blocking JNKs protein phosphorylation.
For example, apigenin has previously been shown to inhibit the growth of human cervical carcinoma cells by inducing apoptosis through a p53-dependant pathway by Zheng et al .
Thus, the employment of apigenin may lead to apoptotic cell death in a variety of tumors.
In our study, we observed that treatment with apigenin led to an increase in the apoptotic cell death of the TC-1 tumor cells (See Figure ).
In the current study, we observed that treatment with apigenin enhanced apoptotic tumor cell death and rendered the TC-1 tumor cells more susceptible to lysis by E7-specific CTLs.
Flow cytometric assays and DNA fragmentation gel electrophoresis also confirmed baicalein induced apoptosis in HL-60 cells.
Taken together, these results suggest that treatment of human leukemia HL-60 cells with baicalein induced apoptosis through activation of caspase-3 activity.
In this study, we evaluated the potential apoptosis effects of baicalein on human promyelocytic leukemia HL-60 cells in vitro.
These results suggested that chrysin-induced apoptosis was likely to be caspase- and mitochondria-dependent, and probably occurs via deregulation of PI3K/Akt, with involvement of XIAP.
In addition, Monasterio et al. [] reported that flavonoids, including chrysin, induced apoptosis via a mechanism that required the activation of caspase-3 and caspase-8, indicating that chrysin-induced apoptosis could act via a ligand receptor-dependent cell death mechanism.
In most of the cancer cells tested, chrysin has shown to inhibit proliferation and induce apoptosis, and is more potent than other tested flavonoids in leukemia cells, where chrysin is likely to act via activation of caspases and inactivation of Akt signaling in the cells.
Therefore, the NFkappaB remains a potential target to study the mechanism of apoptosis induced by chrysin in HeLa cells.
Chrysin inhibits proliferation and induces apoptosis in most cancer cells tested, and is likely more potent than other flavonoids in leukemia cells.
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