DNA Polymerase and Topoisomerase II Inhibitors from <i>Psoralea</i> <i>corylifolia</i>

Sun, Na-Bo; Woo, Seung Hyo; Cassady, John M.; Snapka, Robert M.

doi:10.1021/np970488q

Cited by 239 publications

(80 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It was reported that resveratrol is an inhibitor of ribonucleotid reductase in murine lymphoblastic leukemia cells 16 and an inhibitor of proliferation in K562 human erythroleukemia cells and P815 murine mastocytoma cells 16 and of SV40 replication in CV-1 monkey kidney cells. 17 If such an inhibitory activity holds true for CEM-C7H2 cells as well, it would explain the arrest in S-phase and subsequent induction of apoptosis out of the S-phase. Consistent with our hypothesis is also a report according to which resveratrol is capable of binding to DNA and in the presence of Cu 2+ to cleave DNA.…”

Section: Cell Death and Differentiationmentioning

confidence: 99%

“…12 Although the bioassay for cyclooxygenase I inhibition led to purification of the anticancerogenic agent resveratrol, the mechanisms of anticancerogenicity as well as apoptosis triggering of resveratrol remain unknown. Besides inhibition of cyclooxygenase I, recently discovered antiproliferative effects of resveratrol, such as inhibition of ribonucleotide reductase, 16 inhibition of SV40 DNA replication in CV-1 monkey kidney cells, 17 and other antiproliferative effects, 18 ± 20 may also contribute to the anticancerogenic and apoptosis-inducing properties of resveratrol.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Resveratrol causes arrest in the S-phase prior to Fas-independent apoptosis in CEM-C7H2 acute leukemia cells

et al. 2000

View full text Add to dashboard Cite

Resveratrol (3,5,4'-trihydroxy-trans-stilbene), in the concentration range of 20 mM and above, induced arrest in the Sphase and apoptosis in the T cell-derived T-ALL lymphocytic leukemia cell line CEM-C7H2 which is deficient in functional p53 and p16. Expression of transgenic p16/INK4A, which causes arrest in G0/G1, markedly reduced the percentage of apoptotic cells. Antagonist antibodies to Fas or FasL, or constitutive expression of crmA did not diminish the extent of resveratrol-induced apoptosis. Furthermore, a caspase-8-negative, Fas-resistant Jurkat cell line was sensitive to resveratrol-induced apoptosis which could be strongly inhibited in the Jurkat as well as in the CEM cell line by z-VAD-fmk and z-IETD-fmk. The almost complete inhibition by z-IETD-fmk and the lack of inhibition by crmA suggested caspase-6 to be the essential initiator caspase. Western blots revealed the massive conversion of procaspase-6 to its active form, while caspase-3 and caspase-2 were proteolytically activated to a much lesser extent. Cell Death and Differentiation (2000) 7, 834 ± 842.

show abstract

Section: Cell Death and Differentiationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Resveratrol causes arrest in the S-phase prior to Fas-independent apoptosis in CEM-C7H2 acute leukemia cells

et al. 2000

View full text Add to dashboard Cite

show abstract

“…In -addition to a proapoptotic role, resveratrol has been shown to exhibit antiproliferative effects in various cell types, which may be caused by a dose-dependent inhibition of ribonucleotide reductase activity (Fontecave et al, 1998). Similarly, resveratrol has been found to inhibit DNA polymerase (Sun et al, 1998) as well as ornithine decarboxylase, a key enzyme of polyamine biosynthesis that is enhanced in cancer (Schneider et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

An Analogue of Resveratrol HS-1793 Exhibits Anticancer Activity Against MCF-7 Cells Via Inhibition of Mitochondrial Biogenesis Gene Expression

Jeong

Song

Kim

et al. 2012

Molecules and Cells

View full text Add to dashboard Cite

“…2 Furthermore, it functions as an inhibitor of platelet aggregation, a modulator of lipid and lipoprotein metabolism 3 and an effective blocker of ribonucleotide reductase (ED 50 100 M) that provides deoxyribonucleotides for DNA synthesis. 4 It also inhibits DNA polymerase 5 and mimics estradiol. 6 Several of these activities constitute the basis for the chemopreventive action of resveratrol, exemplified by its antimutagenic activity in the Ames assay, inhibition of tumorigenesis in a 2-stage murine skin-cancer model 2 and inhibition of cell proliferation in vitro.…”

mentioning

confidence: 99%

Resveratrol induces colon tumor cell apoptosis independently of p53 and precede by epithelial differentiation, mitochondrial proliferation and membrane potential collapse

et al. 2001

View full text Add to dashboard Cite

Resveratrol, a polyphenol present in wine and grapes, can inhibit tumor cell growth in vitro and tumorigenesis in vivo. Some of its effects have been linked to activation of the p53 tumor suppressor; however, p53 is frequently mutated in tumors, particularly in the common and often therapy-resistant colon cancers. Using the human wild-type p53-expressing HCT116 colon carcinoma cell line and HCT116 cells with both p53 alleles inactivated by homologous recombination, we show in the current study that resveratrol at concentrations comparable to those found in some foods can induce apoptosis independently of p53. The cell death is primarily mitochondria-mediated and not receptor-mediated. No cells survived in cultures continuously exposed to 100 M resveratrol for 120 hr. When compared with 5-FU, resveratrol stimulated p53 accumulation and activity only weakly and with delayed kinetics and neither the increased levels nor the activity affected apoptosis detectably. The apoptosis agonist Bax was overproduced in response to resveratrol regardless of p53 status, yet the kinetics of Bax expression were influenced by p53. Remarkably, apoptosis was preceded by mitochondrial proliferation and signs of epithelial differentiation. Thus, resveratrol triggers a p53-independent apoptotic pathway in HCT116 cells that may be linked to differentiation. The antifungal phytoalexin resveratrol (3,5,4Ј-trihydroxy-transstilbene) is a constituent of many plant species and present at particularly high levels in grapes and wine. 1 As a polyphenol, it is not only a potent inhibitor of radical formation (ED 50 27 M) but acts as a pleiotropic effector molecule to inhibit initiation, promotion and progression of malignant transformation. Resveratrol inhibits the cyclooxygenase (ED 50 15 M) and hydroperoxidase (ED 50 3.7 M) activities of COX-1 and the hydroperoxidase activity of COX-2 (ED 50 85 M). 2 Furthermore, it functions as an inhibitor of platelet aggregation, a modulator of lipid and lipoprotein metabolism 3 and an effective blocker of ribonucleotide reductase (ED 50 100 M) that provides deoxyribonucleotides for DNA synthesis. 4 It also inhibits DNA polymerase 5 and mimics estradiol. 6 Several of these activities constitute the basis for the chemopreventive action of resveratrol, exemplified by its antimutagenic activity in the Ames assay, inhibition of tumorigenesis in a 2-stage murine skin-cancer model 2 and inhibition of cell proliferation in vitro. 7,8 The presence of the functional wild-type form of the p53 tumor suppressor correlates with the sensitivity of mouse tumors and at least some human tumors to therapeutic agents. 9 -11 p53 is stabilized and activated as a transcription factor in response to a variety of cellular stresses, 12 the result being either cell-cycle arrest, mostly through transcriptional activation of the p21 WAF/Cip1 inhibitor of cyclin-dependent kinases, or apoptosis, depending on the cell context. Apoptosis often involves changes to mitochondria. 13 One of the major predictive parameters indicating commitment...

show abstract

DNA Polymerase and Topoisomerase II Inhibitors from Psoralea corylifolia

Cited by 239 publications

References 22 publications

Resveratrol causes arrest in the S-phase prior to Fas-independent apoptosis in CEM-C7H2 acute leukemia cells

Resveratrol causes arrest in the S-phase prior to Fas-independent apoptosis in CEM-C7H2 acute leukemia cells

An Analogue of Resveratrol HS-1793 Exhibits Anticancer Activity Against MCF-7 Cells Via Inhibition of Mitochondrial Biogenesis Gene Expression

Resveratrol induces colon tumor cell apoptosis independently of p53 and precede by epithelial differentiation, mitochondrial proliferation and membrane potential collapse

Contact Info

Product

Resources

About