Non‐genotoxic environmental carcinogens

Lijinsky, William

doi:10.1080/10590509009373368

Cited by 12 publications

(8 citation statements)

References 55 publications

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“…Some stages in the sequence are not always the same, which means that a number of different overall mechanisms can cause cancer. While mutations often play a role in the multistage nature of carcinogenesis, nongenotoxic mechanisms also play key roles in carcinogenesis [Lijinsky, 1989[Lijinsky, , 1990Holder et al, 1993]. Examples of nongenotoxic mechanistic types are changes in gene expression, cell proliferation, cell organization, cell interrelationhips (including gap junctional intercellular communication), cell death (including apoptosis), and cell removal [Holder et al, 1993].…”

Section: Discussionmentioning

confidence: 99%

Melatonin effects on intercellular junctional communication in MCF‐7 human breast cancer cells

Cos

Fernandez

2000

Journal of Pineal Research

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Melatonin exerts a direct antiproliferative effect on estrogen-responsive MCF-7 cells in culture. Recently, the importance of the anti-invasive actions of melatonin as a part of the oncostatic action of this indolamine has been reported. Gap junctional intercellular communication is known to be involved in controlling cell proliferation and differentiation, and a decrease in intercellular junctional communication has been described in highly invasive mammary cancer cells. Because melatonin at physiological doses (1 nM) shifts MCF-7 cells to a lower invasive status, we postulate that melatonin could modulate the levels of gap junctional intercellular communication in these tumor cells. To test our hypothesis, we studied gap junctional intercellular communication in MCF-7 human breast cancer cells previously (7-8 days) treated, or not, with melatonin (10 microM or 1 nM). Using the scrape-loading assay dye-transfer technique to introduce 0.05% Lucifer yellow into cells, we measured the ability of the tumor cells to transfer dye to adjacent cells. Rhodamine dextran (0.05%) was used as a control dye to verify that dye-transfer occurs through intercellular junctions. The presence of melatonin (10 microM or 1 nM) in the culture medium significantly increased (P < 0.01) the transfer of the dye to adjacent cells through gap junctions. This increase was greater at 10 microM melatonin, and averaged scan profiles of cells treated with melatonin 10 microM showed a statistically significant increase (P < 0.01) in the integrated optical density values, and a broadening of the densitometric scan. These findings suggest that melatonin could exert its antitumor action, at least in part, by increasing regulatory signals that are passed between adjacent epithelial cells through intercellular junctions.

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Section: Discussionmentioning

confidence: 99%

Melatonin effects on intercellular junctional communication in MCF‐7 human breast cancer cells

Cos

Fernandez

2000

Journal of Pineal Research

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“…[15,46,62,69,95,96,118,119,120,148,153,169,206,217,228,283,293,358]; for initiation, promotion and progression see [64,72,88,89,148,158,248,254,255,288,329]; for peroxisome proliferators and oxidative stress see [11,12,18,62,72,82,112,122,128,146,152,195,196,228,268,272,275]; for experimental models see [87,110,113,118,119,120,121,173,241,254]; for membrane bioche...…”

Section: Appendixmentioning

confidence: 99%

“…Each facet of this definition,: randomly chosen from one of the recent papers, has given rise to a very large number of publications which cannot be reviewed here (see Appendix). They have, regrettably, not succeeded in removing "the present state of indecision and uncertainty ..." [206]. For one aspect that is characteristic of our present interpretations of hepatocarcinogenesis is the fact that for every generalization there have been found exceptions, and every explanation attempted has been met by counterarguments.…”

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confidence: 94%

Hepatic neoplasia: reflections and ruminations

Aterman

1995

Vichows Archiv A Pathol Anat

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“…Confusingly, oncogenes may play different roles in different tumors or in different stages of tumorigenesis in the same tumor. Furthermore, many oncogenes may work together in addictive manner [2]. Therefore, it could be of tremendous challenges to investigate the function of a single oncogene in the tumorigenesis and progression with the use of primary cancer tissue.…”

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confidence: 99%

Variation of adhesion capability of K-ras transformed malignant cells and clinical implications

Zhang

Liu

Tan

et al. 2005

Chin. J. Cancer Res.

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Objective: To investigate the mechanism of carcinogenesis, invasion and metastasis. Methods: The expressions of adhesive molecule and adhesive structure in v-k-ras transformed normal rat kidney cells (KNRK) were detected with a variety of molecular biological techniques, including cell culture, immunofluorescence labeling, electron microscopy, polyacrylamide gel electrophoresis, and protein blotting, and compared with normal rat kidney (NRK) cells. Results: The significantly shortened doubling time, remarkably active proliferation ability in soft agar, and invasive growth in the abdomen of nude rat, demonstrated the malignant biological behaviors of KNRK cells. In KNRK cells, the adhesive molecules, P-cadherin, ct and 1~ catenin, actin, and adhesive structures, the adhesive junction and gap junction, were all abnormally expressed. And cell aggregation was significantly decreased. The aggregation ability disappeared at 20°C, and became active with a suitable amount of calcium solution. Conclusion: Following the transfection of virus K-ras gene, normal cells were transformed into malignant cells. In early stage of cancer, the variation of adhesive ability may be one of the vital factors underlying tumorigenesis, invasion and metastasis.

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Non‐genotoxic environmental carcinogens

Cited by 12 publications

References 55 publications

Melatonin effects on intercellular junctional communication in MCF‐7 human breast cancer cells

Melatonin effects on intercellular junctional communication in MCF‐7 human breast cancer cells

Hepatic neoplasia: reflections and ruminations

Variation of adhesion capability of K-ras transformed malignant cells and clinical implications

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