http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
이경호,이다현,김지호,정유정,신순영,고동수,이영한 한국응용생명화학회 2016 Applied Biological Chemistry (Appl Biol Chem) Vol.59 No.3
2-Hydroxy-4-methoxy-2′,3′-benzochalcone (HymnPro), a chalcone derivative, induces cell cycle arrest at the G2/M phase followed by caspase-dependent apoptosis. Structurally, HymnPro contains a α-β olefin that can act as a Michael acceptor, and that is involved in the depletion of cellular glutathione. However, the effect of HymnPro on the generation of reactive oxygen species (ROS) is still unknown. In the present study, we observed that treatment of Capan-1 pancreatic cancer cells with HymnPro resulted in a dose-dependent accumulation of ROS, owing to the depletion of intracellular glutathione. Treatment with ROS scavenger N-acetylcycteine prevented HymnPro-induced caspase activation and cell death, but had little effect on G2/M cell cycle arrest and microtubule assembly. Our results suggest that HymnPro causes tubulin binding-mediated cell cycle arrest at the G2/M phase as well as ROS-mediated caspase activation.
G_2/M phase Arrest and Apoptosis Induction by DW2282 in Human Oral Carcinoma (KB) Cells
Piao, Wenhua,Kwon, Hee-Young,Ha, Jung-Sun,Kim, Yeo-Gab,Kim, Jeong Hee Korean Academy of Oral Biology and the UCLA Dental 2002 International Journal of Oral Biology Vol.27 No.3
We studied the effect of DW2282 on cell proliferation, cell proliferation, cell cycle progression and induction of apoptosis in human oral carcinoma (KB) cells. IC_50 value was determined to be. 0.04㎍/ml. The presence of mRNA synthesis or protein biosynthesis inhibitors did not significantly change IC_50 value of DW2282. Flow-cytometric analysis showed G_2/M phase accumulation then apperarance of subpG_1, apoptotic population. Apoptosis induction was confirmed by fragmentation of DNA in DW2282-treated cells. DW2282 induced-cell cycle arrest was accompanied by decrease in cdc2 and cyclin B1 that have critical roles in progression through the G_2/M phase. We obsered a decreased level of the anti-apoptotic protein Bcl-2, activation of caspase-3 and proteolytic cleavage of poly (ADP-ribose) polymerase. Taken together, our data demonstrate that DW2282 suppresses cell growth by inducing apoptosis after G_2/M phase arrest in KB cells.
Molecular chemotherapeutic potential of butein: A concise review
Jayasooriya, Rajapaksha Gedara Prasad Tharanga,Molagoda, Ilandarage Menu Neelaka,Park, Cheol,Jeong, Jin-Woo,Choi, Yung Hyun,Moon, Dong-Oh,Kim, Mun-Ock,Kim, Gi-Young Elsevier 2018 Food and chemical toxicology Vol.112 No.-
<P><B>Abstract</B></P> <P>Butein is a biologically active flavonoid isolated from the bark of <I>Rhus verniciflua</I> Stokes, which is known to have therapeutic potential against various cancers. Notably, butein inhibits cancer cell growth by inducing G<SUB>2</SUB>/M phase arrest and apoptosis. Butein-induced G<SUB>2</SUB>/M phase arrest is associated with increased phosphorylation of ataxia telangiectasia mutated (ATM) and Chk1/2, and consequently, with reduced cdc25C levels. In addition, butein-induced apoptosis is mediated through the activation of caspase-3, which is associated with changes in the expression of Bcl-2 and Bax proteins. Intriguingly, butein sensitizes cells to tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis via ERK-mediated Sp1 activation, which promotes the transcription of specific death receptor 5. Butein also inhibits the migration and invasion of human cancer cells by suppressing nuclear factor-κB- and extracellular signal-regulated kinases 1/2-mediated expression of matrix metalloproteinase-9 and vascular endothelial growth factor. Additionally, butein downregulates the expression of human telomerase reverse transcriptase and causes a concomitant decrease in telomerase activity. These findings provide the basis for the pharmaceutical development of butein. The aim of this review is to provide an update on the mechanisms underlying the anticancer activity of butein, with a special focus on its effects on different cellular signaling cascades.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Butein induces apoptosis by activating Bax-caspase-3-PARP axis by PI3K/Akt-NF-κB axis through the inhibition of ROS generation. </LI> <LI> Butein induces G<SUB>2</SUB>/M phase cell cycle arrest by inhibiting ROS-mediated ATM-Chk1/2-Cdc25c-cdc2/cyclin B axis. </LI> <LI> Butein enhances TRAIL-mediated apoptosis by increasing DR5 expression through ERK-mediated Sp1 activation. </LI> <LI> Butein suppresses telomerase activity by inhibiting TERT expression and phosphorylation via c-Myc and PI3K/Akt. </LI> <LI> Butein attenuates angiogenesis, invasion/metastasis, and inflammation by suppressing the NF-κB signal pathway. </LI> </UL> </P>
Li, Ge,Kim, Dong-Hee,Kim, Tae-Dong,Park, Byoung-Jeon,Park, Hae-Duck,Park, Jong-Il,Na, Min-Kyun,Kim, Hwan-Chul,Hong, Nam-Doo,Lim, Kyu,Hwang, Byung-Doo,Yoon, Wan-Hee 충남대학교 암연구소 2005 암연구소 업적집 Vol.4 No.-
The cytotoxic mechanism of protein-bound polysaccharide isolated from Phellinus linteus (PL, Mesim_(?)) has been investigated. PL inhibited the proliferation and colony formation of SW480 human colon cancer cells. Flow cytometry analysis showed that PL increased the populations of both apoptotic sub-G_(1) and G_(2)/M phase. The result obtained from TUNEL assay corroborated apoptosis which was shown in flow cytometry. Western blot analysis suggested that PL-induced apoptosis and growth inhibition were associated with decrease in Bcl-2, increase of the release of cytochrome c, and reduced expression of cyclin B1. These results suggest that PL has a direct antitumor effect through apoptosis and cell cycle blockade in certain cancer cells.
Li, Ge,Kim, Dong-Hee,Kim, Tae-Dong,Park, Byoung-Jeon,Park, Hae-Duck,Park, Jong-Il,Na, Min-Kyun,Kim, Hwan-Chul,Hong, Nam-Doo,Lim, Kyu,Hwang, Byung-Doo,Yoon, Wan-Hee 충남대학교 암공동연구소 2005 암공동연구소 업적집 Vol.4 No.
The cytotoxic mechanism of protein-bound polysaccharide isolated from Phellinus linteus (PL, Mesim_(??)) has been investigated. PL inhibited the proliferation and colony formation of SW480 human colon cancer cells. Flow cytometry analysis showed that PL increased the populations of both apoptotic sub-G_(1) and G_(2)/M phase. The result obtained from TUNEL assay corroborated apoptosis which was shown in flow cytometry. Western blot analysis suggested that PL-induced apoptosis and growth inhibition were associated with decrease in Bcl-2, increase of the release of cytochrome c, and reduced expression of cyclin B1. These results suggest that PL has a direct antitumor effect through apoptosis and cell cycle blockade in certain cancer cells.
이형주 서울대학교 농업개발연구소 2000 농업생명과학연구 Vol.4 No.-
An anticancer peptide from soy protein was purified and isolated. Defatted soy protein was hydrolyzed with thermoase and its hydrophobic peptides were extracted with ethanol. The peptide extract was fractionated by XAD-2 adsorption, gel filtration chromatography, and different C18 HPLCs. Anticancer activity of each fraction was assayed by measuring in vitro cytotoxicity on P388D1, a mouse monocyte macrophage cell line. IC50 value of a peptide fraction from Sephadex G-25 chromatography was 0.16 mg/ml. This peptide fraction at 1 mg/ml significantly affected cell cycle progression by arresting P388D1 at G2/M phases. Finally purified peptide from analytical C18 HPLC was nonapeptide of which molecular weight was 1157 Da and the sequence was X-Met-Leu-Pro-Ser-Tyr-Ser-Pro-Tyr.
Vitexicarpin Induces Apoptosis in Human Prostate Carcinoma PC-3 Cells through G2/M Phase Arrest
Meng, Fan-Min,Yang, Jing-Bo,Yang, Chun-Hui,Jiang, Yu,Zhou, Yong-Feng,Yu, Bo,Yang, Hong Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.12
Vitexicarpin (3', 5-dihydroxy-3, 4', 6, 7-tetramethoxyflavone), a polymethoxyflavone isolated from Viticis Fructus (Vitex rotundifolia Linne fil.), has long been used as an anti-inflammatory herb in traditional Chinese medicine. It has also been reported that vitexicarpin can inhibit the growth of various cancer cells. However, there is no report elucidating its effect on human prostate carcinoma cells. The aim of the present study was to examine the apoptotic induction activity of vitexicarpin on PC-3 cells and molecular mechanisms involved. MTT studies showed that vitexicarpin dose-dependently inhibited growth of PC-3 cells with an $IC_{50}{\sim}28.8{\mu}M$. Hoechst 33258 staining further revealed that vitexicarpin induced apoptotic cell death. The effect of vitexicarpin on PC-3 cells apoptosis was tested using prodium iodide (PI)/Annexin V-FITC double staining and flow cytometry. The results indicated that vitexicarpin induction of apoptotic cell death in PC-3 cells was accompanied by cell cycle arrest in the G2/M phase. Furthermore, our study demonstrated that vitexicarpin induction of PC-3 cell apoptosis was associated with upregulation of the proapoptotic protein Bax, and downregulation of antiapoptotic protein Bcl-2, release of Cytochrome c from mitochondria and decrease in mitochondrial membrane potential. Our findings suggested that vitexicarpin may become a potential leading drug in the therapy of prostate carcinoma.