Aloe emodin decreases the ERK-dependent anticancer activity of cisplatin
Само за регистроване кориснике
2005
Аутори
Mijatovic, SMaksimovic-Ivanic, D
Radovic, J
Miljković, Đorđe
Kaludjerovic, GN
Sabo, Tibor
Trajković, Vladimir S.
Чланак у часопису (Објављена верзија)
Метаподаци
Приказ свих података о документуАпстракт
The present study describes the ability of an anthraquinone derivative aloe emodin (AE) to reduce the cytotoxic activity of the platinum(II)-based anticancer agent cisplatin toward murine L929 fibrosarcoma and C6 glioma cell lines. The protective effect of AE was demonstrated by MTT and crystal violet assays for cell viability, and involved supression of cisplatin-induced apoptosis and necrosis, as assessed by lactate dehydrogenase release and flow cytometric analysis of DNA fragmentation or phosphatidylserine exposure. Cell-based ELISA and Western blot analysis revealed that AE abolished cisplatin-triggered activation of extracellular signal-regulated kinase (ERK) in tumor cells, while activation of c-Jun N-terminal kinase was not significantly altered. A selective blockade of ERK activation with PD98059 mimicked the protective effect of AE treatment in both tumor cell lines. Moreover, AE failed to protect tumor cells against the ERK-independent toxicity of the Pt(IV)-based complex te...trachloro(O,O-dibutyl-ethylenediamine-N,N'-di-3-propanoate)platinum(IV). Taken together, these data indicate that herbal anthraquinone AE can downregulate the anticancer activity of cisplatin by blocking the activation of ERK in tumor cells.
Кључне речи:
aloe emodin / cisplatin / ERK / apoptosis / necrosis / cancerИзвор:
Cellular and Molecular Life Sciences / CMLS, 2005, 62, 11, 1275-1282Издавач:
- Birkhauser Verlag Ag, Basel
DOI: 10.1007/s00018-005-5041-3
ISSN: 1420-682X
PubMed: 15905960
WoS: 000232496800009
Scopus: 2-s2.0-21144443656
Колекције
Институција/група
Hemijski fakultet / Faculty of ChemistryTY - JOUR AU - Mijatovic, S AU - Maksimovic-Ivanic, D AU - Radovic, J AU - Miljković, Đorđe AU - Kaludjerovic, GN AU - Sabo, Tibor AU - Trajković, Vladimir S. PY - 2005 UR - https://cherry.chem.bg.ac.rs/handle/123456789/733 AB - The present study describes the ability of an anthraquinone derivative aloe emodin (AE) to reduce the cytotoxic activity of the platinum(II)-based anticancer agent cisplatin toward murine L929 fibrosarcoma and C6 glioma cell lines. The protective effect of AE was demonstrated by MTT and crystal violet assays for cell viability, and involved supression of cisplatin-induced apoptosis and necrosis, as assessed by lactate dehydrogenase release and flow cytometric analysis of DNA fragmentation or phosphatidylserine exposure. Cell-based ELISA and Western blot analysis revealed that AE abolished cisplatin-triggered activation of extracellular signal-regulated kinase (ERK) in tumor cells, while activation of c-Jun N-terminal kinase was not significantly altered. A selective blockade of ERK activation with PD98059 mimicked the protective effect of AE treatment in both tumor cell lines. Moreover, AE failed to protect tumor cells against the ERK-independent toxicity of the Pt(IV)-based complex tetrachloro(O,O-dibutyl-ethylenediamine-N,N'-di-3-propanoate)platinum(IV). Taken together, these data indicate that herbal anthraquinone AE can downregulate the anticancer activity of cisplatin by blocking the activation of ERK in tumor cells. PB - Birkhauser Verlag Ag, Basel T2 - Cellular and Molecular Life Sciences / CMLS T1 - Aloe emodin decreases the ERK-dependent anticancer activity of cisplatin VL - 62 IS - 11 SP - 1275 EP - 1282 DO - 10.1007/s00018-005-5041-3 ER -
@article{ author = "Mijatovic, S and Maksimovic-Ivanic, D and Radovic, J and Miljković, Đorđe and Kaludjerovic, GN and Sabo, Tibor and Trajković, Vladimir S.", year = "2005", abstract = "The present study describes the ability of an anthraquinone derivative aloe emodin (AE) to reduce the cytotoxic activity of the platinum(II)-based anticancer agent cisplatin toward murine L929 fibrosarcoma and C6 glioma cell lines. The protective effect of AE was demonstrated by MTT and crystal violet assays for cell viability, and involved supression of cisplatin-induced apoptosis and necrosis, as assessed by lactate dehydrogenase release and flow cytometric analysis of DNA fragmentation or phosphatidylserine exposure. Cell-based ELISA and Western blot analysis revealed that AE abolished cisplatin-triggered activation of extracellular signal-regulated kinase (ERK) in tumor cells, while activation of c-Jun N-terminal kinase was not significantly altered. A selective blockade of ERK activation with PD98059 mimicked the protective effect of AE treatment in both tumor cell lines. Moreover, AE failed to protect tumor cells against the ERK-independent toxicity of the Pt(IV)-based complex tetrachloro(O,O-dibutyl-ethylenediamine-N,N'-di-3-propanoate)platinum(IV). Taken together, these data indicate that herbal anthraquinone AE can downregulate the anticancer activity of cisplatin by blocking the activation of ERK in tumor cells.", publisher = "Birkhauser Verlag Ag, Basel", journal = "Cellular and Molecular Life Sciences / CMLS", title = "Aloe emodin decreases the ERK-dependent anticancer activity of cisplatin", volume = "62", number = "11", pages = "1275-1282", doi = "10.1007/s00018-005-5041-3" }
Mijatovic, S., Maksimovic-Ivanic, D., Radovic, J., Miljković, Đ., Kaludjerovic, G., Sabo, T.,& Trajković, V. S.. (2005). Aloe emodin decreases the ERK-dependent anticancer activity of cisplatin. in Cellular and Molecular Life Sciences / CMLS Birkhauser Verlag Ag, Basel., 62(11), 1275-1282. https://doi.org/10.1007/s00018-005-5041-3
Mijatovic S, Maksimovic-Ivanic D, Radovic J, Miljković Đ, Kaludjerovic G, Sabo T, Trajković VS. Aloe emodin decreases the ERK-dependent anticancer activity of cisplatin. in Cellular and Molecular Life Sciences / CMLS. 2005;62(11):1275-1282. doi:10.1007/s00018-005-5041-3 .
Mijatovic, S, Maksimovic-Ivanic, D, Radovic, J, Miljković, Đorđe, Kaludjerovic, GN, Sabo, Tibor, Trajković, Vladimir S., "Aloe emodin decreases the ERK-dependent anticancer activity of cisplatin" in Cellular and Molecular Life Sciences / CMLS, 62, no. 11 (2005):1275-1282, https://doi.org/10.1007/s00018-005-5041-3 . .