Differential effects of calcium deprivation on the cytoskeleton of non-tumorigenic and tumorigenic rat liver cells in culture

Swierenga, S.H.H.; Goyette, René; Marceau, Normand

doi:10.1016/0014-4827(84)90446-4

Cited by 19 publications

(7 citation statements)

References 27 publications

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“…The CK redistribution in some cells resembled that of cultured Morris hepatoma cells (Fig. 7b, Swierenga et al, 1984); and with long-term maintenance with SB (to 4 months), cells both with and without Ni escaped the DNA synthesis block and acquired a marked morphological transformed phenotype ( Fig. 7d,e; these cells were not tested for GGT or tumor induction in nude mice).…”

Section: Resultsmentioning

confidence: 88%

“…CK39, found in bile duct cells in vivo is only weakly expressed, as determined by immunofluorescence (not shown); and unlike duct cells in vivo, T51B cells do not express GGT (Marceau et al, 1986). The hepatocyte cytokeratin CK49 (Franke et al, 1981; is absent; vimentin is present (Swierenga et al, 1984).…”

Section: Resultsmentioning

confidence: 93%

“…For immunofluorescence staining, cells were fixed in cold acetone or ethanol and processed as described previously (Swierenga et al, 1984).…”

Section: Methodsmentioning

confidence: 99%

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Altered cytokeratin expression and differentiation induction during neoplastic transformation of cultured rat liver cells by nickel subsulfide

et al. 1989

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Rat liver T51B cells were maintained in the presence of low concentrations of Ni(II) derived from alpha Ni3S2 for 3-15 months in culture in order to monitor cytokeratin, differentiation, and transformation patterns. Nickel exposures caused irreversible, heritable juxtanuclear aggregates of cytokeratin CK55, which increased in size and complexity with prolonged nickel exposure, eventually resembling Mallory bodies and expressing glutamyltransferase. Altered cytokeratin expression was accompanied by induction of differentiation, with markers of both bile ductular cells and hepatocytes, such as induction of cytokeratin polypeptides CK39 and CK49, cell morphology, and cytokeratin filament network changes; whereas control cultures similarly maintained for long periods in culture remained unchanged. Altered cytokeratin expression was also accompanied by acquisition of transformation markers--loss of density dependence, progression toward calcium independence, and (benign) growth in nude mice. Observed cytokeratin aberrations may be a factor in nickel carcinogenesis, in view of the known affinity of the metal for cellular structural proteins, especially keratin, which play a role in maintenance of cell behavior.

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Section: Resultsmentioning

confidence: 88%

Section: Resultsmentioning

confidence: 93%

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Altered cytokeratin expression and differentiation induction during neoplastic transformation of cultured rat liver cells by nickel subsulfide

et al. 1989

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“…Strong evidence suggests that Ca2 + plays an important role in the triggering of mitogen induced cell proliferation in a number of types of cells Tsien et al, 1982a;Moolenaar et al, 1984) and that calcium might be important in regulating cell differentiation (Bridges et al, 1981). These observations are supported by other studies demonstrating that culture medium containing low Ca2 + ion concentrations retards the growth of normal cells while allowing the proliferation of transformed cells (Veigl et al 1984).…”

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confidence: 90%

The free cytoplasmic calcium concentration of tumorigenic and non-tumorigenic human somatic cell hybrids

Banyard¹,

Tellam²

1985

Br J Cancer

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Summary The fluorescent indicator of Ca2 + concentration, quin-2, has been used to measure the concentration of free Ca2 + in the cytoplasm of tumorigenic and non-tumorigenic human somatic cell hybrids. The cell hybrids were derived from the fusion of a HeLa derivative (D98 AH2) and normal human fibroblasts. The calcium concentration of the tumorigenic cell lines was 180+7nM and the level in the nontumorigenic cells was 136+6nM. This difference was statistically highly significant (P<0.001). Control experiments are reported which show that the level of 3a2+ measured is not influenced by cell density or by the concentration of quin-2-tetra-(acetoxymethyl)ester used in these experiments. The possible implications of this elevated level of cytoplasmic calcium in tumorigenic cells are discussed.

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“…Furthermore, differential effects oc cur between normal and initiated cells as is indicated by the switch in the flowchart. Tu mor cell lines respond in a totally different fashion in that they do not terminally differ entiate even with high [Ca2+]c [37], Thus, ionophores or any modification of [CA2+]e can exert a differential effect on normal ver sus initiated cells. Such is suspected to be at least one mechanism of tumor promotion.…”

Section: Cytoskeletal-mediated Effectsmentioning

confidence: 99%

The Role of Calcium in Cell Injury and Repair: A Hypothesis

Trump¹,

Berezesky²

1985

Pathol Immunopathol Res

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Differential effects of calcium deprivation on the cytoskeleton of non-tumorigenic and tumorigenic rat liver cells in culture

Cited by 19 publications

References 27 publications

Altered cytokeratin expression and differentiation induction during neoplastic transformation of cultured rat liver cells by nickel subsulfide

Altered cytokeratin expression and differentiation induction during neoplastic transformation of cultured rat liver cells by nickel subsulfide

The free cytoplasmic calcium concentration of tumorigenic and non-tumorigenic human somatic cell hybrids

The Role of Calcium in Cell Injury and Repair: A Hypothesis

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