Polyamines and prostatic cancer

2003 ◽  
Vol 31 (2) ◽  
pp. 375-380 ◽  
Author(s):  
R.G. Schipper ◽  
J.C. Romijn ◽  
V.M.J.I. Cuijpers ◽  
A.A.J. Verhofstad
Keyword(s):  
Cell Growth ◽  
Cancer Cells ◽  
Ornithine Decarboxylase ◽  
Prostatic Cancer ◽  
Apoptotic Cell ◽  
Metabolic Enzymes ◽  
Human Prostate ◽  
In Vivo Model ◽  
Biological Behaviour ◽  
Polyamine Analogues

The importance of polyamines in prostatic growth and differentiation has prompted studies to evaluate the clinical relevance of the ornithine decarboxylase/polyamine system in prostatic cancer. These studies show that differences in biological behaviour of prostatic (cancer) cells are associated with changes in polyamine levels and/or the activity of their metabolic enzymes. Faulty antizyme regulation of polyamine homoeostasis may play an important role in the growth and progression of prostatic carcinoma. Treatment of human prostate carcinoma cells with inhibitors of polyamine metabolic enzymes or polyamine analogues induces cell growth arrest or (apoptotic) cell death. Our recent in vitro studies using conformationally restricted polyamine analogues show that these compounds inhibit cell growth, probably by inducing antizyme-mediated degradation of ornithine decarboxylase. Sensitivity of human prostate cancer cells for these compounds was increased in the absence of androgens. These results suggest that these analogues might have chemotherapeutic potential in case prostatic cancer has become androgen-independent. Pilot data in an in vivo model show that these analogues have effects on tumour cell proliferation, vascularity, blood perfusion and tissue hypoxia. Overall, these studies show that polyamines may serve as important biomarkers of prostatic malignancy and provide a promising target for chemotherapy of prostatic cancer.

scholarly journals Investigations of the mechanism by which mammalian cell growth is inhibited by N1N12-bis(ethyl)spermine

1993 ◽  
Vol 291 (1) ◽  
pp. 131-137 ◽  
Author(s):  
L Albanese ◽  
R J Bergeron ◽  
A E Pegg
Keyword(s):  
Mitochondrial Dna ◽  
Cell Growth ◽  
Cell Lines ◽  
Ornithine Decarboxylase ◽  
Polyamine Analogues ◽  
Proliferative Effect ◽  
L1210 Cells ◽  
Inhibition Of Growth ◽  
Variant Cell ◽  
Mammalian Cell Growth

N1N12-Bis(ethyl)spermine (BESM) and related compounds are powerful inhibitors of cell growth that may have potential as anti-neoplastic agents [Bergeron, Neims, McManis, Hawthorne, Vinson, Bortell and Ingeno (1988) J. Med. Chem. 31, 1183-1190]. The mechanism by which these compounds bring about their effects was investigated by using variant cell lines in which processes thought to be altered by these agents are perturbed. Comparisons between the response of these cells and of their parental equivalents to BESM, N1N11-bis(ethyl)norspermine, N1N14-bis(ethyl)homospermine and N1N8-bis(ethyl)spermidine were then made. It was found that D-R cells, an L1210-derived line that over-expresses ornithine decarboxylase, were not resistant to these compounds. This indicates that the decrease in ornithine decarboxylase is not critical for the action of the compounds on cell growth. Furthermore, although polyamine levels were decreased in the D-R cells, the content was not totally depleted, indicating that such depletion is also not essential for the anti-proliferative effect. Two cell lines lacking mitochondrial DNA (human 143B206 cells and chicken DU3 cells) did not differ in sensitivity to BESM from their parental 143BTK- and DU24 cells. Furthermore, the inhibition of respiration in L1210 cells in response to BESM developed more slowly than the inhibition of growth. Thus it appears that the inhibitions of mitochondrial DNA synthesis and of mitochondrial respiration are also not primary factors in the anti-proliferative effects of these polyamine analogues. The inhibition of growth did, however, correlate with the intracellular accumulation of the analogues. It appears that the bis(ethyl)polyamine derivatives act by binding to intracellular target molecules and preventing macromolecular synthesis. The decline in normal polyamines may facilitate such binding, but is not essential for growth arrest.

Blueberry flavonoids inhibit matrix metalloproteinase activity in DU145 human prostate cancer cells

2005 ◽  
Vol 83 (5) ◽  
pp. 637-643 ◽  
Author(s):  
Michael D Matchett ◽  
Shawna L MacKinnon ◽  
Marva I Sweeney ◽  
Katherine T Gottschall-Pass ◽  
Robert A.R Hurta
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Human Prostate ◽  
Response To Treatment ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
The Matrix ◽  
Ecm Degradation

Regulation of the matrix metalloproteinases (MMPs), the major mediators of extracellular matrix (ECM) degradation, is crucial to regulate ECM proteolysis, which is important in metastasis. This study examined the effects of 3 flavonoid-enriched fractions (a crude fraction, an anthocyanin-enriched fraction, and a proanthocyanidin-enriched fraction), which were prepared from lowbush blueberries (Vaccinium angustifolium), on MMP activity in DU145 human prostate cancer cells in vitro. Using gelatin gel electrophoresis, MMP activity was evaluated from cells after 24-hr exposure to blueberry fractions. All fractions elicited an ability to decrease the activity of MMP-2 and MMP-9. Of the fractions tested, the proanthocyanidin-enriched fraction was found to be the most effective at inhibiting MMP activity in these cells. No induction of either necrotic or apoptotic cell death was noted in these cells in response to treatment with the blueberry fractions. These findings indicate that flavonoids from blueberry possess the ability to effectively decrease MMP activity, which may decrease overall ECM degradation. This ability may be important in controlling tumor metastasis formation.Key words: blueberry flavonoids, MMP activity, prostate cancer cells.

scholarly journals Endoplasmic reticulum stress, autophagic and apoptotic cell death, and immune activation by a natural triterpenoid in human prostate cancer cells

2018 ◽  
Vol 120 (4) ◽  
pp. 6264-6276 ◽  
Author(s):  
Benjamin M. Johnson ◽  
Faisal F. Y. Radwan ◽  
Azim Hossain ◽  
Bently P. Doonan ◽  
Jessica D. Hathaway‐Schrader ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Endoplasmic Reticulum Stress ◽  
Cancer Cells ◽  
Immune Activation ◽  
Apoptotic Cell ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells

Truncated Lactoferricin peptide controls cervical cancer cell proliferation via lncRNA-NKILA/NF-κB feedback loop

2021 ◽  
Vol 28 ◽  
Author(s):  
Yuan Pan ◽  
Yuting Jiang ◽  
Yingli Cui ◽  
Jihong Zhu ◽  
Yang Yu
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Feedback Loop ◽  
Apoptotic Cell ◽  
Cervical Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Cervical Cancer Cells

Background : Lactoferricin peptide (LP) has been reported to control cancer cell proliferation. NF‐κB interacting lncRNA (NKILA) is a tumor suppressor in several cancers. Objective: We aimed to explore the potential function of the truncated LP (TLP) in the prevention of cervical cancer cell proliferation. Methods: Bioinformatics analysis via PPA-Pred2 showed that 18-aa N-terminus of truncated lactoferricin peptide (TLP18, FKCRRWQWRMKKLGAPSI) shows higher affinity with nuclear factor kappaB (NF-κB) than LP. The effects of LP and TLP18 on cervical cancer cells SiHa and HeLa and the related mechanisms were explored by investigating NF‐κB and lncRNA-NKILA. Results : TLP18 shows an inhibitory rate up to 0.4-fold higher than LP on the growth of cervical cancer cells (P<0.05). NKILA siRNA promoted cell growth whether LP or TLP18 treatment (P<0.05). TLP18 treatment increases the level of lncRNA-NKILA and reduces the level of NF‐κB up to 0.2-fold and 0.6-fold higher than LP (P<0.05), respectively. NKILA siRNA increased the levels of NF‐κB, cleaved caspase-3, and BAX (P<0.05). TLP18 increased apoptotic cell rate up to 0.2-fold higher than LP, while NKILA siRNA inhibited cell apoptosis cell growth even LP or TLP18 treatment. Conclusion: Truncated Lactoferricin peptide controls cervical cancer cell proliferation via lncRNA-NKILA/NF‐κB feedback loop.

A humanized tissue-engineered in vivo model to dissect interactions between human prostate cancer cells and human bone

2014 ◽  
Vol 31 (4) ◽  
pp. 435-446 ◽  
Author(s):  
Parisa Hesami ◽  
Boris M. Holzapfel ◽  
Anna Taubenberger ◽  
Martine Roudier ◽  
Ladan Fazli ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Human Bone ◽  
Human Prostate ◽  
In Vivo Model ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells

scholarly journals Dual action of NSC606985 on cell growth and apoptosis mediated through PKCδ in prostatic cancer cells

2017 ◽  
Vol 51 (5) ◽  
pp. 1601-1610 ◽  
Author(s):  
Xin Wang ◽  
Chen Tan ◽  
Guo Wang ◽  
Jing-Jing Cai ◽  
Li-Ping Wang ◽  
...  
Keyword(s):  
Cell Growth ◽  
Cancer Cells ◽  
Prostatic Cancer ◽  
Dual Action
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