Enhancement of chemotherapeutic agent-induced apoptosis by inhibition of NF-κB using ursolic acid

2010 ◽  
pp. NA-NA ◽  
Author(s):  
Yunlong Li ◽  
Da Xing ◽  
Qun Chen ◽  
Wei R. Chen
Keyword(s):  
Ursolic Acid ◽  
Chemotherapeutic Agent ◽  
Induced Apoptosis

scholarly journals Inhibition of Caspases Inhibits the Release of Apoptotic Bodies: Bcl-2 Inhibits the Initiation of Formation of Apoptotic Bodies in Chemotherapeutic Agent-induced Apoptosis

1999 ◽  
Vol 145 (1) ◽  
pp. 99-108 ◽  
Author(s):  
Jiandi Zhang ◽  
Mary C. Reedy ◽  
Yusuf A. Hannun ◽  
Lina M. Obeid
Keyword(s):  
Cell Death ◽  
Chemotherapeutic Agent ◽  
Chromatin Condensation ◽  
Membrane Lipid ◽  
Lymphoid Cells ◽  
Parp Cleavage ◽  
Apoptotic Bodies ◽  
Normal Morphology ◽  
Release Assay ◽  
Induced Apoptosis

During apoptosis, the cell actively dismantles itself and reduces cell size by the formation and pinching off of portions of cytoplasm and nucleus as “apoptotic bodies.” We have combined our previously established quantitative assay relating the amount of release of [3H]-membrane lipid to the degree of apoptosis with electron microscopy (EM) at a series of timepoints to study apoptosis of lymphoid cells exposed to vincristine or etoposide. We find that the [3H]-membrane lipid release assay correlates well with EM studies showing the formation and release of apoptotic bodies and cell death, and both processes are regulated in parallel by inducers or inhibitors of apoptosis. Overexpression of Bcl-2 or inhibition of caspases by DEVD inhibited equally well the activation of caspases as indicated by PARP cleavage. They also inhibited [3H]-membrane lipid release and release of apoptotic bodies. EM showed that cells overexpressing Bcl-2 displayed near-normal morphology and viability in response to vincristine or etoposide. In contrast, DEVD did not prevent cell death. Although DEVD inhibited the chromatin condensation, PARP cleavage, release of apoptotic bodies, and release of labeled lipid, DEVD-treated cells showed accumulation of heterogeneous vesicles trapped in the condensed cytoplasm. These results suggest that inhibition of caspases arrested the maturation and release of apoptotic bodies. Our results also imply that Bcl-2 regulates processes in addition to caspase activation.

scholarly journals PGV-0 AND PGV-1 INCREASED APOPTOSIS INDUCTION OF DOXORUBICIN ON MCF-7 BREAST CANCER CELLS

2015 ◽  
Vol 12 (2) ◽  
pp. 55-59
Author(s):  
Edy Meiyanto
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Chemotherapeutic Agent ◽  
Apoptosis Induction ◽  
Single Treatment ◽  
Cell Cycle Modulation ◽  
Induced Apoptosis ◽  
Mcf 7

As chemotherapeutic backbone for breast cancer therapy, doxorubicin showed various side effects and induced resistancy of breast cancer cells. Development of targeted therapy on breast cancer focused on combinatorial therapy of doxorubicin and molecular targeted agents. PGV-0 and PGV-1, a curcumin analogue showed potency as co-chemotherapeutic agent with doxorubicin. Our previous study of PGV-0 and PGV-1 showed cytotoxic activity in T47D cells. Therefore, the aim of this research is to examine the synergistic effect of PGV-0, PGV-1 on the cytotoxic activity of doxorubicin through cell cycle modulation and apoptotic induction on MCF-7 breast cancer cell lines. The cytotoxic assay of PGV-0, PGV-1, doxorubicin, and their combination were carried out by using MTT assay. Cell cycle distribution and apoptosis were determined by flowcytometer FACS-Calibur and the flowcytometry data was analyzed using Cell Quest program. Single treatment of PGV-0, PGV-1 and doxorubicin showed cytotoxic effect on MCF-7 with cell viability IC50 value 50 µM, 6 µM and 350 nM respectively. Single treatment of Doxorubicin 175 nM induced G2/M arrest. Single treatment of PGV-0 5 µM induced G2/M arrest while in higher dose 12.5  µM, PGV-0 induced apoptosis. Combination of doxorubicin 175 nM and PGV-0 5 µM induced apoptosis. Combination of doxorubicin 175 nM and PGV-0 12.5 µM also increased apoptosis induction. Single treatment of PGV-1 0.6 µM induced G1 arrest while in higher dose 1.5  µM, PGV-1 induced apoptosis. Combination of doxorubicin 175 nM and PGV-1 0.6 µM induced apoptosis. Combination of doxorubicin 175 nM and PGV-0 1.5 µM also increased apoptosis induction. PGV-0 and PGV-1 are potential to be delevoped as co-chemotherapeutic agent for breast cancer by inducing apoptosis and cell cycle modulation, but the molecular mechanism need to be explored detail.  Key words: PGV-0, PGV-1, doxorubicin, co-chemotherapy, breast cancer, cell cycle arrest, apoptosis

Resistance to ursolic acid-induced apoptosis through involvement of melanogenesis and COX-2/PGE2 pathways in human M4Beu melanoma cancer cells

2016 ◽  
Vol 345 (1) ◽  
pp. 60-69 ◽  
Author(s):  
Lama Hassan ◽  
Aline Pinon ◽  
Youness Limami ◽  
Josiane Seeman ◽  
Chloe Fidanzi-Dugas ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Ursolic Acid ◽  
Melanoma Cancer ◽  
Cox 2 ◽  
Induced Apoptosis

Inactivation of Beclin-1-dependent autophagy promotes ursolic acid-induced apoptosis in hypertrophic scar fibroblasts

2017 ◽  
Vol 27 (1) ◽  
pp. 58-63 ◽  
Author(s):  
Chuan Cao ◽  
Wenping Wang ◽  
Lele Lu ◽  
Liang Wang ◽  
XiaoSong Chen ◽  
...  
Keyword(s):  
Ursolic Acid ◽  
Hypertrophic Scar ◽  
Beclin 1 ◽  
Induced Apoptosis

scholarly journals Secang (Caesalpinia sappan L.) Heartwood Ethanolic Extract Shows Activity as Doxorubicin Co-chemotherapeutic Agent by Apoptotis Induction on T47D Breast Cancer Cells

2012 ◽  
Vol 3 (2) ◽  
pp. 376 ◽  
Author(s):  
Ika Nurzijah ◽  
Dyaningtyas Dewi Pamungkas Putri ◽  
Erlina Rivanti ◽  
Edy Meiyanto
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Chemotherapeutic Agent ◽  
Annexin V ◽  
Ethanolic Extract ◽  
Multi Drug Resistance ◽  
Caesalpinia Sappan ◽  
T47d Cells ◽  
Induced Apoptosis

Doxorubicin, primary chemoteurapeutic agent used for breast cancer treatment, is known to have various side effects included multi drug resistance (MDR) phenomenon. Therefore, exploration of co-chemotherapeutic agent is important to be conducted in order to prevent MDR. Secang (Caesalpinia sappan L.) which contains active compounds brazilin and brazilein, is proven to have activity as anticancer. The aim of this study is to determine the potency of Caesalpinia sappan L. ethanolic extract (CEE) as co-chemotherapeutic agent of doxorubicin and its mechanism through apoptosis induction on T47D breast cancer cells. Caesalpinia sappan L. heartwood powder was macerated with ethanol 70%. The cytotoxic effect of CEE alone and its combination with doxorubicin was analyzed using MTT assay. Apoptosis assay was done by flowcytometry-annexin V method. CEE showed cytotoxic activity on T47D cells with IC50 value of 35 µg/ml, while combinatorial test showed that all of combination doses of CEE and doxorubicin gave synergistic effect. Flowcytometry-annexin V assay proved that treatment of CEE induced apoptosis of doxorubicin. Based on these results, we conclude that Caesalpinia sappan L. heartwood ethanolic extract is potential to be developed as co-chemotherapeutic agent of doxorubicin.Keywords : Caesalpinia sappan L., doxorubicin, apoptosis, T47D cells

scholarly journals Design, Synthesis, and Biological Evaluation of Novel Nitrogen Heterocycle-Containing Ursolic Acid Analogs as Antitumor Agents

Molecules ◽  
2019 ◽  
Vol 24 (5) ◽  
pp. 877 ◽  
Author(s):  
Wenzhi Wang ◽  
Lei Lei ◽  
Zhi Liu ◽  
Hongbo Wang ◽  
Qingguo Meng
Keyword(s):  
Cell Lines ◽  
Ursolic Acid ◽  
Antitumor Agents ◽  
Biological Evaluation ◽  
Nitrogen Heterocycle ◽  
Mitochondrial Potential ◽  
Design Synthesis ◽  
Induced Apoptosis ◽  
Mkn45 Cell

Nineteen ursolic acid analogues were designed, synthesized, and evaluated for their antiproliferative activity against the Hela and MKN45 cell lines. Some compounds containing a piperazine moiety displayed moderate to high levels of antitumor activities against the tested cancer cell lines. The most potent compound shares the IC50 value of 2.1 µM and 2.6 µM for the Hela and MKN45 cell lines, respectively. Further mechanism studies and in vivo antitumor studies have shown that it decreased the apoptosis regulator (BCL2/BAX) ratio, disrupted mitochondrial potential and induced apoptosis, and suppressed the growth of Hela xenografts in nude mice.

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