| 1. |
- Edgren, M, et al.
(författare)
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Serum concentrations of VEGF and b-FGF in renal cell, prostate and urinary bladder carcinomas.
- 1999
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Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 19:1B, s. 869-73
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Tidskriftsartikel (refereegranskat)abstract
- Sixty nine patients with urogenital cancers (renal, bladder and prostate cancer) were studied to determine whether the serum concentrations of Vascular Endothelial Growth Factor (VEGF) and basic Fibroblast Growth Factor (b-FGF) reflected the status of the patients and/or the prognosis of the disease. Of the patients included in this study, renal cell carcinoma patients expressed the highest levels of VEGF indicating that these tumours are more VEGF dependent. The values of b-FGF could be considered normal in all three malignancies. No correlation was observed between the expression of VEGF and b-FGF, nor between VEGF and b-FGF and patients survival.
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| 2. |
- Ishihara, M., et al.
(författare)
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Quantitative structure-cytotoxicity relationship analysis of phenoxazine derivatives by semiempirical molecular-orbital method
- 2007
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Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 27:6B, s. 4053-4057
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Tidskriftsartikel (refereegranskat)abstract
- A semiempirical molecular-orbital method (CAChe) was applied to delineate the relationship between the cytotoxicity (evaluated by 50% cytotoxic concentration, CC50) of fifteen phenoxazine derivatives and eleven physical parameters (descriptors). Most of the phenoxazine derivatives had extended and planar structure. The cytotoxic activity of phenoxazines against the human oral squamous cell carcinoma HSC-2 and HSC-4 cells correlated to electron affinity, absolute hardness (eta), absolute electron negativity (chi) and octanol-water distribution coefficient (log-P). However, only log-P was correlated to CC50 in the HSC-3 cells, whereas only heat of formation and log-P were correlated to CC50 in the human promyelocytic leukemia HL-60 cells. The cytotoxic activity of the phenoxazine derivatives became maximum at the log-P=5.9. Their cytotoxicity strongly depended on the chi value, but not on the eta value. Compounds with relatively higher cytotoxicity showed higher chi value (chi > 5.28), whereas compounds with relatively lower cytotoxicity showed lower chi value (chi < 4.27). These data suggest that appropriate chemical descriptors should be selected to estimate the cytotoxicity of phenoxazines, depending on the target cells.
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| 3. |
- Karlsson, Sandra, et al.
(författare)
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Inhibition of CYP27B1 and CYP24 Increases the Anti-proliferative Effects of 25-Hydroxyvitamin D 3 in LNCaP Cells
- 2021
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Ingår i: Anticancer Research. - : Anticancer Research USA Inc.. - 0250-7005 .- 1791-7530. ; 41:10, s. 4733-4740
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Tidskriftsartikel (refereegranskat)abstract
- Background/Aim: Growing evidence suggests that vitamin D3 exerts anticancer effects. The present study aimed to evaluate 25-hydroxyvitamin D3(25(OH)D3) as a potential endocrine factor regulating proliferation and vitamin D receptor expression in LNCaP prostate cancer cells. Materials and Methods: Cell counting after treatment was utilized to assess the effect of 25(OH)D3on cell proliferation. Changes in mRNA expression of the vitamin D receptors, VDR and PDIA3, were evaluated using droplet digital polymerase chain reaction (ddPCR). Results: 25(OH)D3inhibited cell proliferation in a dose- and time-dependent manner. The inhibitory effect of 25(OH)D3on cell proliferation was potentiated after inhibition of CYP17B1 and CYP24 by genistein, preventing further metabolism of 25(OH)D3to 1,25-dihydroxyvitamin D3(1,25(OH)2D3) and 24,25-dihydroxyvitamin D3(24,25(OH)2D3). Expression of PDIA3 and VDR mRNA increased after treatment with 25(OH)D3, whereas the ratio between PDIA3 and VDR mRNA remained unchanged. Conclusion: 25(OH)D3has a direct inhibitory effect on cell proliferation, which is enhanced and accelerated when the metabolism of 25(OH)D3to 1,25(OH)2D3and 24,25(OH)2D3was inhibited by the CYP17B1 and CYP24 inhibitor genistein. Furthermore, treatment with 25(OH)D3increased receptor transcript expression, suggesting an increased VDR stability and sensibility of the treated cells.
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| 4. |
- Suzuki, F., et al.
(författare)
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Tumor-specificity and type of cell death induced by phenoxazines
- 2007
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Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 27:6B, s. 4233-4238
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Tidskriftsartikel (refereegranskat)abstract
- Phenoxazines have shown diverse biological activities, but tumor-specific cytotoxic activity has not been investigated. A total of 24 phenoxazine derivatives (WM1-24) was investigated for their relative cytotoxicity against human tumor cell lines vs. normal cells. WM7 and WM8 showed the highest tumor-specificity index of 4.3 and 4.8, respectively. Considerable difference in drug-sensitivity was found among these tumor cell lines. Human promyelocytic leukemia HL-60 cells showed the highest sensitivity to both WM7 and WM8, followed by human oral squamous cell carcinoma (HSC-2, HSC-3, HSC-4), and human gingival fibroblast (HGF), pulp cell (HPC) and periodontal ligament fibroblast (HPLF) were the most resistant. WM7 and WM8 induced little or no internucleosomal DNA fragmentation, and activated caspase-3 in HSC-2, HSC-4 and human glioblastoma T98G cells. These compounds failed to induce autophagic cell death, as judged by acridine orange and microtubule-associated protein I light chain 3 (LC3)-GFP assays. These results suggested that the higher cytotoxicity of WM7 and WM8 are derived from the positively-charged quaternary nitrogen substituents on the phenoxazine ring and the electron density of nitrogen at N12, and that inhibition of autophagy is not always coupled with apoplosis induction.
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