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1

Defective brca2 influences topoisomerase I activity in mammalian cells

100%

Rahden-Staron I., Szumilo M., Grosicka E., Kraakman-van der Zwet M., Zdzienicka M. Z.

Acta Biochimica Polonica

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2003

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tom 50

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nr 1

The Chinese hamster cell mutant V-C8 is defective in the Brca2 gene (Kraakman-van der Zwet et al., 2002, Cell Biol.-, 22: 669). Here we report that V-C8 cells were 10-fold more sensitive to camptothecin, an inhibitor of topoisomerase I, than the parental V79 cells. The level of the relaxation activity of topoisomerase I in nuclear extracts was also lower (4-fold) in V-C8 than V79 cells, in spite of the fact that the level of the topoisomerase I protein was the same in these cells. The survival of V-C8 cells in the presence of camptothecin, the sensitivity of V-C8 topoisomerase I to camptothecin, and the level of the relaxation activity in V-C8 nuclear extract were almost completely restored by transfection of V-C8 cells with the murine Brca2 gene or by the transfer of human chromosome 13 providing the BRCA2 gene. These results indicate that the observed changes in the topoisomerase I activity in V-C8 are due to the defective function of the Brca2 gene.

2

Cytoprotective effect of lithium against spontaneous and induced apoptosis of lymphoid cell line MOLT-4

84%

Pietruczuk K., Jozwik A., Ruckemann-Dziurdzinska K., Bryl E., Witkowski J. M.

Folia Histochemica et Cytobiologica

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2009

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tom 47

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nr 4

3

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Phytochemical and pharmacological aspects of Nothapodytes nimmoniana. An overview

84%

Khan N., Tamboli E. T., Sharma V. K., Kumar S.

Herba Polonica

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2013

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tom 59

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nr 1

Nothapodytes nimmoniana (J. Graham) (Icacinaceae), commonly known as Amruta is found in India particularly in Maharashtra, Goa, Kerala, Assam, Jammu and Kashmir as well as Tamilnadu areas. It is an important medicinal plant, the major source of a potent alkaloid, namely camptothecin, of a wide spectrum of pharmacological activities like anti-cancer, anti-HIV, antimalarial, antibacterial, anti-oxidant, anti-inflammatory, anti-fungal and also applied in the treatment of anaemia. Camptothecin is still not synthesized, therefore, its production entirely depends on natural sources. N. nimmoniana is one such plant which yields contain camptothecin in significantly high amount. The plant is gaining international recognition due to its diversified medicinal uses. It is subjected to excessive harvest. It has been categorized as a vulnerable and endangered plant. The present review encompasses the phytochemical, analytical, pharmacological, biotechnological, and other specific aspects of N. nimmoniana.

4

A quinone-containing compound enhances camptothecin-Induced apoptosis of lung cancer through modulating endogenous ROS and ERK signaling

84%

Chou H.-L., Fong Y., Wei C.-K., Tsai E.-M., Chen J. Y.-F., Chang W.-T., Wu C.-Y., Huang H.-W., Chiu C.-C.

Archivum Immunologiae et Therapiae Experimentalis

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2017

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tom 65

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nr 3

5

Cathepsins and BID are involved in the molecular switch between apoptosis and autophagy in breast cancer MCF-7 cells exposed to camptothecin

84%

Lamparska-Przybysz M., Gajkowska B., Motyl T.

Journal of Physiology and Pharmacology. Supplement

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2005

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tom 56

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nr 3

159-179

The details of molecular switching points between apoptosis and autophagy in tumor cells have still not been fully elucidated. This study focused on the role of cathepsin B and its substrate, BID as molecular links between apoptosis and autophagy in human breast cancer MCF-7 cells exposed to camptothecin. Apoptosis occurred rapidly with a peak in 60 min after drug administration, whereas autophagy developed at a much slower rate with continuous progression during 24 h of cell exposure to the drug. CPT induced very rapid activation of cathepsin B. Inhibition of cathepsins by E64d prevented CPT-induced BAX and BID aggregation on mitochondria and reduced significantly reduced apoptotic cell number. The above effects were accompanied by an increase in autophagosome formation, measured by expression of MAP I LC3. BID knock down resulted in strong suppression of CPT-induced apoptosis and a shift of cell death towards autophagy, manifesting with an increase of Beclin 1 and MAP I LC3 cellular content.

6

Translocation of apoptosis-related proteins in MCF-7 cells exposed to camptothecin in the mitochondrial pathway of apoptosis

84%

Gajkowska B., Wojewodzka U., Walski M., Frontczak-Baniewicz M.

Acta Biologica Cracoviensia. Series Zoologia

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2003

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tom 45

7

Camptothecin induces the transit of FasL trimers to the cell surface in apoptosis HEp-2 cells

84%

Meza-Lamas E., Bollain-Y-Goytia J.J., Ramirez-Sandoval R., Sanchez-Rodriguez S. H., Lopez-Robles E., Avaloz-Diaz E., Herrera-Esparza R.

Cellular and Molecular Biology Letters

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2006

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tom 11

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nr 3

Fas ligand (L) is a membrane protein from the tumor necrosis factor (TNF) family. It induces apoptosis upon contact with its Fas/CD95/APO1 receptor. Trimerization of FasL on the surface of effector cells is essential in the binding of the Fas trimer of the target cells. The receptor then recruits an adaptor and caspase-like proteins which lead apoptosis. This paper reports on the fate of FasL in HEp-2 cells committed to apoptosis by induction with campthotecin. Our main results demonstrated that in non-apoptotic cells, FasL aggregates in the cytoplasm forming trimers of 120 kDa. Apoptosis increases the trimeric FasL species, but also induces its dissociation into monomers of 35 kDa. In conclusion, camptothecin appears to perturb the Fas and FasL segregation in the cytoplasm by promoting the transit of FasL to the cell surface, thus fostering a process of autocrine or paracrine apoptosis. FasL is trimerized prior to Fas/FasL complex formation, and after apoptosis, FasL undergoes an intense turnover.

8

The diverse effect of topoisomerase I specific inhibitor [ camptothecin ] on normal and BCR-ABL - dependent hematopoietic cells proliferation: therapeutic implications

84%

Fertala J., Nieborowska-Skorska M., Calabretta B., Skorski T.

Folia Histochemica et Cytobiologica

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1995

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tom 33

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nr 3

9

Toxin- and cadmium-induced cell death events in tomato suspension cells resemble features of hypersensitive response

67%

Iakimova E. T., Woltering E. J., Yordanova Z. P.

Journal of Fruit and Ornamental Plant Research

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2007

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tom 15

10

Pharmacological inhibition of GSK3 attenuates DNA damage-induced apoptosis via reduction of p53 mitochondrial translocation and Bax oligomerization in neuroblastoma SH-SY5Y cells

59%

Ngok-Ngam P., Watcharasit P., Thiantanawat A., Satayavivad J.

Cellular and Molecular Biology Letters

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2013

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tom 18

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nr 1

Glycogen synthase kinase-3 (GSK3) and p53 play crucial roles in the mitochondrial apoptotic pathway and are known to interact in the nucleus. However, it is not known if GSK3 has a regulatory role in the mitochondrial translocation of p53 that participates in apoptotic signaling following DNA damage. In this study, we demonstrated that lithium and SB216763, which are pharmacological inhibitors of GSK3, attenuated p53 accumulation and caspase-3 activation, as shown by PARP cleavage induced by the DNA-damaging agents doxorubicin, etoposide and camptothecin. Furthermore, each of these agents induced translocation of p53 to the mitochondria and activated the mitochondrial pathway of apoptosis, as evidenced by the release of cytochrome C from the mitochondria. Both mitochondrial translocation of p53 and mitochondrial release of cytochrome C were attenuated by inhibition of GSK3, indicating that GSK3 promotes the DNA damage-induced mitochondrial translocation of p53 and the mitochondrial apoptosis pathway. Interestingly, the regulation of p53 mitochondrial translocation by GSK3 was only evident with wild-type p53, not with mutated p53. GSK3 inhibition also reduced the phosphorylation of wild-type p53 at serine 33, which is induced by doxorubicin, etoposide and camptothecin in the mitochondria. Moreover, inhibition of GSK3 reduced etoposide-induced association of p53 with Bcl2 and Bax oligomerization. These findings show that GSK3 promotes the mitochondrial translocation of p53, enabling its interaction with Bcl2 to allow Bax oligomerization and the subsequent release of cytochrome C. This leads to caspase activation in the mitochondrial pathway of intrinsic apoptotic signaling.

Ograniczanie wyników

Defective brca2 influences topoisomerase I activity in mammalian cells

Cytoprotective effect of lithium against spontaneous and induced apoptosis of lymphoid cell line MOLT-4

Phytochemical and pharmacological aspects of Nothapodytes nimmoniana. An overview

A quinone-containing compound enhances camptothecin-Induced apoptosis of lung cancer through modulating endogenous ROS and ERK signaling

Cathepsins and BID are involved in the molecular switch between apoptosis and autophagy in breast cancer MCF-7 cells exposed to camptothecin

Translocation of apoptosis-related proteins in MCF-7 cells exposed to camptothecin in the mitochondrial pathway of apoptosis

Camptothecin induces the transit of FasL trimers to the cell surface in apoptosis HEp-2 cells

The diverse effect of topoisomerase I specific inhibitor [ camptothecin ] on normal and BCR-ABL - dependent hematopoietic cells proliferation: therapeutic implications

Toxin- and cadmium-induced cell death events in tomato suspension cells resemble features of hypersensitive response

Pharmacological inhibition of GSK3 attenuates DNA damage-induced apoptosis via reduction of p53 mitochondrial translocation and Bax oligomerization in neuroblastoma SH-SY5Y cells