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Wyświetlanie 1-2 z 2
Tytuł:
SIRT3-SOD2-ROS pathway is involved in linalool-induced glioma cell apoptotic death
Autorzy:
Cheng, Yanhao
Dai, Chao
Zhang, Jian
Powiązania:
https://bibliotekanauki.pl/articles/1038661.pdf
Data publikacji:
2017
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
linalool
glioma
apoptotic cell death
SIRT3
SOD2
Opis:
Glioma is the most prevalent type of adult primary brain tumor and chemotherapy of glioma was limited by drug-resistance. Linalool is an acyclic monoterpene alcohol possessing various pharmacological activities. The present study was conducted to evaluate the effect of linalool on glioma cell growth. The effect of linalool on cell viability in U87-MG cells was investigated and the results showed that linalool significantly reduced cell viability in a concentration- and time-dependent manner. In addition, exposure of the cells to linalool resulted in a concentration-dependent increase of TUNEL-stained cells, indicating the occurrence of apoptotic cell death. Linalool decreased mitochondrial oxygen consumption rate, increased the expression of Bax and Bak, reduced the expression of Bcl-2 and Bcl-xl, and increased the activities of caspase 3 and caspase 9, leading to increase of apoptosis. Linalool resulted in a concentration-dependent decrease of SOD activity but had no significant effect on mRNA and protein expression of SOD2. Moreover, linalool resulted in a significant increase of the expression of acetylated SOD2. The mRNA and protein expression of SIRT3 was significantly inhibited by linalool. Immunoblot analysis showed that there was an evident protein/protein interaction between SOD2 and SIRT3 under normal condition. Linalool treatment significantly decreased the interaction between SOD2 and SIRT3. Overexpression of SIRT3 significantly inhibited linalool-induced increase of mitochondrial ROS production and apoptotic cell death, and decrease of cell viability. In summary, the data demonstrated that linalool exhibited inhibitory effect on glioma cells through regulation of SIRT3-SOD2-ROS signaling.
Źródło:
Acta Biochimica Polonica; 2017, 64, 2; 343-350
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Comparative analysis of RCAS1 level in neoplasms and placenta.
Autorzy:
Wicherek, Lukasz
Dutsch, Magdalena
Mak, Pawel
Klimek, Marek
Skladzien, Jacek
Dubin, Adam
Powiązania:
https://bibliotekanauki.pl/articles/1043411.pdf
Data publikacji:
2003
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
EBAG9
RCAS1
immune escape
apoptotic cell death
fetal rejection
Opis:
The tumor associated antigen RCAS1 (receptor-binding cancer antigen expressed on SiSo cells) expressed with high frequency in various cancer and trophoblast cells, inhibits growth of estrogen receptor-expressing cells and induces apoptosis. Because previous reports demonstrated RCAS1 presence only by non-quantitative immunocytochemistry methods, we decided to use a Western blotting with anti-RCAS1 monoclonal antibodies for estimation of the relative content of the tumor-associated antigen. One hundred tissue samples were assayed (neoplasms, chronic inflammatory diseases, healthy tissues, trophoblasts and placentas at term). RCAS1 was present in all neoplastic, placental and trophoblast tissue samples and its level in malignant samples was statistically significantly higher than in benign neoplasms. The amount of RCAS1 in chronic inflammations was also significantly increased in immune mediated diseases, like allergic nasal polyps and sarcoidosis. The RCAS1 protein was not revealed in healthy mucous membrane and in muscle tissues. The presented results suggest that RCAS1 might play an important role in tumor escape from host immunological surveillance and carry weight in the down regulation of the maternal immune response, thereby maintaining pregnancy.
Źródło:
Acta Biochimica Polonica; 2003, 50, 4; 1187-1194
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
    Wyświetlanie 1-2 z 2

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