Inhibition of proliferation and apoptosis of human and rat T lymphocytes by curcumin, a curry pigment

Sikora, Ewa; Bielak-Żmijewska, Anna; Piwocka, Katarzyna; Skierski, Janusz; Radziszewska, Ewa

doi:10.1016/s0006-2952(97)00251-7

Cited by 100 publications

(50 citation statements)

References 40 publications

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“…Induction of prosurvival and antiapoptotic genes Curcumin-mediated radiosensitivity D Chendil et al strongly suggests that PC-3 cells harbor a tight regulatory loop that inhibits the cell killing effects of ionizing radiation. Curcumin has been reported to be a potent antiproliferative agent for many tumor types (Rao et al, 1995;Sikora et al, 1997) and it acts as a proapoptotic agent in a variety of cancer cell lines (Kuo et al, 1996;Khar et al, 1999). Exposure of PC-3 cells to curcumin inhibited radiation-induced Bcl-2 expression, indicating that radiation-induced TNF-a is necessary to activate NFkB, which is required for the induction of Bcl-2 protein.…”

Section: Discussionmentioning

confidence: 99%

Curcumin confers radiosensitizing effect in prostate cancer cell line PC-3

et al. 2004

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Curcumin (Diferuloylmethane) is a major chemical component of turmeric (curcuma longa) and is used as a spice to give a specific flavor and yellow color in Asian food. Curcumin exhibits growth inhibitory effects in a broad range of tumors as well as in TPA-induced skin tumors in mice. This study was undertaken to investigate the radiosensitizing effects of curcumin in p53 mutant prostate cancer cell line PC-3. Compared to cells that were irradiated alone (SF 2 ¼ 0.635; D 0 ¼ 231 cGy), curcumin at 2 and 4 lM concentrations in combination with radiation showed significant enhancement to radiation-induced clonogenic inhibition (SF 2 ¼ 0.224: D 0 ¼ 97 cGy and SF 2 ¼ 0.080: D 0 ¼ 38 cGy) and apoptosis. It has been reported that curcumin inhibits TNF-a-induced NFjB activity that is essential for Bcl-2 protein induction. In PC-3 cells, radiation upregulated TNF-a protein leading to an increase in NFjB activity resulting in the induction of Bcl-2 protein. However, curcumin in combination with radiation treated showed inhibition of TNF-a-mediated NFjB activity resulting in bcl-2 protein downregulation. Bax protein levels remained constant in these cells after radiation or curcumin plus radiation treatments. However, the downregulation of Bcl-2 and no changes in Bax protein levels in curcumin plus radiation-treated PC-3 cells, together, altered the Bcl2 : Bax ratio and this caused the enhanced radiosensitization effect. In addition, significant activation of cytochrome c and caspase-9 and -3 were observed in curcumin plus radiation treatments. Together, these mechanisms strongly suggest that the natural compound curcumin is a potent radiosesitizer, and it acts by overcoming the effects of radiation-induced prosurvival gene expression in prostate cancer.

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Section: Discussionmentioning

confidence: 99%

Curcumin confers radiosensitizing effect in prostate cancer cell line PC-3

et al. 2004

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“…STAT5 is proposed to be the main determinant of Bcr-Abl-dependent cyclin D2 overexpression, and it could be a curcumin target (36,37). Moreover, the cyclin D2 gene promoter contains binding sites for the activator protein-1 and nuclear factor-nB transcription factors, and curcumin inhibits their DNA-binding activity (36,38).…”

Section: Discussionmentioning

confidence: 99%

Curcumin Affects Components of the Chromosomal Passenger Complex and Induces Mitotic Catastrophe in Apoptosis-Resistant Bcr-Abl-Expressing Cells

Wolanin

Magalska

Mosieniak

et al. 2006

Molecular Cancer Research

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The Bcr-Abl oncoprotein plays a major role in the development and progression of chronic myeloid leukemia and is a determinant of chemotherapy resistance occurring during the blast crisis phase of the disease. The aim of this article was to investigate the possibility of combating the resistance to apoptosis caused by Bcr-Abl by inducing an alternative cell death process. As a model of chronic myeloid leukemia, we employed Bcr-Abl-transfected mouse progenitor 32D cells with low and high Bcr-Abl expression levels corresponding to drug-sensitive and drug-resistant cells, respectively. The drug curcumin (diferuloylmethane), a known potent inducer of cell death in many cancer cells, was investigated for efficacy with Bcr-Abl-expressing cells. Curcumin strongly inhibited cell proliferation and affected cell viability by inducing apoptotic symptoms in all tested cells; however, apoptosis was a relatively late event. G 2 -M cell cycle arrest, together with increased mitotic index and cellular and nuclear morphology resembling those described for mitotic catastrophe, was observed and preceded caspase-3 activation and DNA fragmentation. Mitosis-arrested cells displayed abnormal chromatin organization, multipolar chromosome segregation, aberrant cytokinesis, and multinucleated cellsmorphologic changes typical of mitotic catastrophe. We found that the mitotic cell death symptoms correlated with attenuated expression of survivin, a member of the chromosomal passenger complex, and mislocalization of Aurora B, the partner of survivin in the chromosomal passenger complex. Inhibition of survivin expression with small interfering RNA exhibited similar mitotic disturbances, thus implicating survivin as a major, albeit not the only, target for curcumin action.This study shows that curcumin can overcome the broad resistance to cell death caused by expression of Bcr-Abl and suggests that curcumin may be a promising agent for new combination regimens for drug-resistant chronic myeloid leukemia.

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“…It is very well known that curcumin can influence many cell functions by targeting transcriptional activities. [21][22][23] Curcumin is a well-known inhibitor of NFjB transcription factor, 8 which recently has been recognized as transcriptional activator of survivin. 24 To further support the hypothesis that survivin decrease is due to NFjB inhibition, we analyzed 2 other very well-recognized NFjB targets, namely Bcl-2 and XIAP, 25 and found that the protein level of both genes resulted to be decreased in curcumin-but not vincristine-treated cells.…”

Section: Discussionmentioning

confidence: 99%

Resistance to apoptosis of HCW‐2 cells can be overcome by curcumin‐ or vincristine‐induced mitotic catastrophe

Magalska

Śliwińska

Szczepanowska

et al. 2006

Intl Journal of Cancer

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The term mitotic catastrophe has recently become widely used to describe a form of death affecting many cancer cells, which, because of severe DNA or mitotic spindle damage, are not able to bypass mitosis. We show here that cells of the HL-60-derived HCW-2 line highly resistant to apoptosis, upon treatment with curcumin or vincristine, undergo mitotic catastrophe that is finalized by caspase 3 activation and oligonucleosomal DNA degradation. Curcumin is a natural dye, derived from Curcuma longa that has been shown to induce cell death in many cancer cells. Both treatments decrease cell proliferation and cell survival, arrest cells in G 2 /M phase of cell cycle and induce morphological changes characterized by cell enlargement and micronucleation. ''Catastrophic'' cells comprise a separate subpopulation with less than 4 C DNA, as evidenced by flow and scanning cytometry. This subpopulation is MPM-2 positive. Thymidine block increased the number of cell arrested in the G 2 /M phase of cell cycle and curcumin effectiveness as an inducer of mitotic catastrophe. Curcumin, but not vincristine, acts on HCW-2 cells by inhibiting the expression of survivin, a modulator of cell division and apoptosis in cancer. Altogether our results show that apoptosis resistance can be overcome by inducing mitotic catastrophe in HCW-2 cells. ' 2006 Wiley-Liss, Inc.

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Inhibition of proliferation and apoptosis of human and rat T lymphocytes by curcumin, a curry pigment

Cited by 100 publications

References 40 publications

Curcumin confers radiosensitizing effect in prostate cancer cell line PC-3

Curcumin confers radiosensitizing effect in prostate cancer cell line PC-3

Curcumin Affects Components of the Chromosomal Passenger Complex and Induces Mitotic Catastrophe in Apoptosis-Resistant Bcr-Abl-Expressing Cells

Resistance to apoptosis of HCW‐2 cells can be overcome by curcumin‐ or vincristine‐induced mitotic catastrophe

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