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PubMed1985

Neoplastic transformation of mast cells by Abelson-MuLV: abrogation of IL-3 dependence by a nonautocrine mechanism.

Normal mast cells can be propagated in culture when medium is supplemented with interleukin-3 (IL-3). We demonstrate that Abelson-MuLV (Ab-MuLV) infection of mast cells eliminates dependence on IL-3 for growth. By contrast, Harvey, BALB, and Moloney MSV, which also productively infect mast cells, are unable to relieve IL-3 dependence. Ab-MuLV-induced IL-3-independent lines express the v-abl-specific transforming protein and have phenotypic characteristics of mast cells. These cells also possess high cloning efficiencies in soft agarose and are tumorigenic in nude mice. In addition, Ab-MuLV induces transplantable mastocytomas in pristane-primed adult mice resistant to lymphoid transformation, defining a new hematopoietic target for malignant transformation by this virus. None of the Ab-MuLV-derived transformants express or secrete detectable levels of IL-3 nor is their growth inhibited by anti-IL-3 serum. These results argue that Ab-MuLV abrogation of the IL-3 requirement is not due to an autocrine mechanism.

Abelson murine leukemia virus↗
PubMed2002

Inhibition of glycolipid shedding rescues recognition of a CD1+ T cell lymphoma by natural killer T (NKT) cells.

Neoplastic transformation of cells is accompanied by an aberration of cell surface glycolipid composition. These tumor-associated, altered glycosphingolipids are often shed into the tumor cell microenvironment and mediate immunosuppressive activity. The nature and form of glycolipids shed by a variety of tumor cell lines and the mechanism(s) of shedding have been well characterized. The murine T cell lymphoma line, L5178Y-R, is known to shed a tumor-associated glycolipid, gangliotriaosylceramide, into the culture medium. We analyzed the effect of glycolipids from L5178Y-R on antigen presentation by murine CD1d1 molecules. CD1d1 molecules present glycolipid antigens to a specialized class of T cells called natural killer T (NKT) cells that mainly express a T cell receptor alpha chain (Valpha14Jalpha281) associated with Vbeta chains of limited diversity. In the current report, we found that L5178Y-R cells express CD1 on their cell surface yet are unable to stimulate CD1d1-specific NKT cells. We hypothesized that the glycolipid(s) shed by L5178Y-R inhibited antigen presentation by CD1d1. Pretreatment of CD1d1(+) cells with conditioned medium from L5178Y-R inhibited CD1-specific stimulation of canonical (Valpha14(+)) but not noncanonical (Valpha5(+)) NKT cells. Exogenous addition of lipids extracted from L5178Y-R cells as well as purified gangliotriaosylceramide mimicked this effect. Inhibition of glycolipid shedding in L5178Y-R cells with d-1-phenyl-2-hexadecanoylamino-3-morpholino-1-propanol resulted in the rescue of CD1d1 recognition by canonical (but not noncanonical) NKT cells. These results suggest that one means by which certain tumor cells can evade the host's innate antitumor immune response is by shedding glycolipids that inhibit CD1-mediated antigen presentation to NKT cells.

Animals↗
PubMed1996

Localization and function of the connexin 43 gap-junction protein in normal and various oncogene-expressing rat liver epithelial cells.

Clones of rat liver epithelial cells genotypically altered by mutation or by a variety of oncogenes were analyzed by microinjection-dye transfer, immunofluorescence confocal microscopy, and western blotting to determine at what level and to what degree these transformations disrupted gap-junctional intercellular communication (GJIC) mediated by connexin 43 (Cx43). Compared with normal rat liver epithelial cells, cells neoplastically transformed by src, neu, ras, and myc/ras all displayed reduced degrees of GJIC, reduced levels of membrane-associated Cx43 plaques, and hypophosphorylation of Cx43. Confocal analysis further demonstrated that the Cx43 protein was localized, at least in part, to the nucleus rather than to the plasma membrane in the src- and neu-transformed cells, but not in the ras- and myc/ras-transformed cells. Nuclei isolated from WB-neu cells showed substantially higher levels of Cx43 on western blotting than did nuclei from WB-neo control cells, supporting the idea that the nuclear-localized immunopositive material detected by confocal microscopy was Cx43 protein. In a GJIC-deficient mutant rat liver epithelial cell line containing normal numbers of plasma membrane-localized Cx43 plaques that appeared to be reduced in size, the Cx43 protein was also found to be hypophosphorylated. Cells overexpressing myc, on the other hand, displayed a normal degree of GJIC, increased levels of plasma membrane-localized Cx43 plaques, and hyperphosphorylation of the Cx43 protein. Cells expressing raf, previously shown to be GJIC competent, showed Cx43 immunostaining patterns similar to those in normal cells, whereas a cell line established from a tumor induced by injection of these raf-expressing cells into a mouse showed a marked reduction in GJIC and plasma membrane-associated Cx43 immunostaining. These data suggest that altered localization of the gap-junction protein Cx43, mediated in part by changes in the phosphorylation of this protein, contributes to the disruption of GJIC in neoplastically transformed rat liver epithelial cells.

Animals↗
PubMed2002

Enhanced neoplastic transformation by mammography X rays relative to 200 kVp X rays: indication for a strong dependence on photon energy of the RBE(M) for various end points.

The fundamental assumption implicit in the use of the atomic bomb survivor data to derive risk estimates is that the gamma rays of Hiroshima and Nagasaki are considered to have biological efficiencies equal to those of other low-LET radiations up to 10 keV/microm, including mammography X rays. Microdosimetric and radiobiological data contradict this assumption. It is therefore of scientific and public interest to evaluate the efficiency of mammography X rays (25-30 kVp) to induce cancer. In this study, the efficiency of mammography X rays relative to 200 kVp X rays to induce neoplastic cell transformation was evaluated using cells of a human hybrid cell line (CGL1). For both radiations, a linear-quadratic dose-effect relationship was observed for neoplastic transformation of CGL1 cells; there was a strong linear component for the 29 kVp X rays. The RBE(M) of mammography X rays relative to 200 kVp X rays was determined to be about 4 for doses < or = 0.5 Gy. A comparison of the electron fluences for both X rays provides strong evidence that electrons with energies of < or = 15 keV can induce neoplastic transformation of CGL1 cells. Both the data available in the literature and the results of the present study strongly suggest an increase of RBE(M) for carcinogenesis in animals, neoplastic cell transformation, and clastogenic effects with decreasing photon energy or increasing LET to an RBE(M) approximately 8 for mammography X rays relative to 60Co gamma rays.

Animals↗
PubMed1983

The role of calmodulin in the proliferation of transformed and phenotypically normal tsASV-infected rat cells.

NRK cells infected with a temperature-sensitive, transformation-defective mutant of avian sarcoma virus (ASV), tsLA23, behaved as if nontransformed at a nonpermissive 40 degrees C and were rendered quiescent by serum deprivation. These serum-deprived cells were stimulated to start entering S phase about 7 hours after serum addition at 40 degrees C or about 9 hours after shifting the cultures to 36 degrees C, a temperature allowing the production of active viral pp60src and expression of the transformed phenotype. The transit of both serum- and temperature-stimulated tsLA23-NRK cells through later G1 was inhibited by the unrelated calmodulin antagonists W7 and R24571. The former drug was found to block the cells at a point in the cell cycle no more than 2 hours from the G1/S transition. The weaker calmodulin antagonist, W5, was less effective in impairing progression. Thus, calmodulin is likely required for the transit of both transformed and phenotypically normal tsLA23-NRK cells through the later stages of their G1 phases. Cells neoplastically transformed by ASV contain more calmodulin than uninfected, non-neoplastic cells. At the nonpermissive 40 degrees C, the calmodulin content of the tsLA23-NRK cells dropped to the non-neoplastic level. When these phenotypically nontransformed cells were enabled to reenter the cell cycle while still in low-serum medium by a 40 to 36 degrees C shift, they passed through the G1 and S phases and divided without a concomitant rise in the total calmodulin content. Thus, a calmodulin rise does not appear to be required for the expression of one characteristic of transformed cells, i.e., reduced requirement for exogenous growth factors.

Animals↗
PubMed2002

Enhanced mutation and neoplastic transformation in human cells by 29 kVp relative to 200 kVp X rays indicating a strong dependence of RBE on photon energy.

The fundamental assumption implicit in the use of the atomic bomb survivor data to derive risk estimates for occupational and medical exposures is that the gamma rays of Hiroshima and Nagasaki are considered as equal efficiencies to other low LET radiations up to an LET of 10 keV.micron-1. For breast cancer induction, neoplastic cell transformation, mutation, reciprocal translocations and dicentrics in human lymphocytes, a strong and very similar dependence of the RBE values on photon energy or on LET is observed. Experimental data on mutation induction and neoplastic cell transformation in human cells show that 29 kVp X rays are by a factor of 4 and 3.4, respectively, more effective compared with 200 kVp X rays. These data are in excellent agreement with the data in the literature.

Cell Transformation, Neoplastic↗
PubMed1993

Radiation-induced neoplastic transformation of human cells.

Ionizing radiation can induce cancers in humans and animals and can cause in vitro neoplastic transformation of various rodent cell systems. However, numerous attempts to achieve neoplastic transformation of human cells by radiation have generally proven unsuccessful. Neoplastic transformation of immortalized human epidermal keratinocytes by X-ray irradiation has recently been reported. The carcinogenic effect of radiation on cultured human cells will be briefly reviewed. The current state-of-the-art in radiation-induced transformation of human cells in culture is presented. This will provide insight into the molecular and cellular mechanisms in the conversion of normal cells to a neoplastic state of growth.

Cell Transformation, Neoplastic↗
PubMed1995

Comparison of propylene oxide and epichlorohydrin effects in two transformation tests (C3H/10T1/2 and SHE cells).

The neoplastic cell transformation induced by propylene oxide (PO) and epichlorohydrin (ECH) was studied in two in vitro assays, mouse embryo fibroblasts (C3H/10T1/2) and Syrian hamster embryo (SHE) cells. In C3H/10T1/2 cells treated with PO (2.5-10 mM), the transformation frequencies were enhanced about 2-4 times in the presence of 12-O-tetradecanoylphorbol-13-acetate (TPA), compared with the transformation frequencies in the absence of TPA. In SHE cells, an even higher increase (about 6-9 times) was reached at concentrations of 2.5-20 mM. The presence of TPA strongly influenced the ability of ECH to induce the morphological transformation at low-moderate concentrations (0.25-1 mM). At the highest concentrations applied, 1 mM in C3H/10T1/2 cells and 0.5 mM in SHE cells, 41- and 4-fold increases, respectively, were observed. In C3H/10T1/2 cells, the rad-equivalence (rad/mMh) of PO and ECH in the presence of TPA was calculated to be 36 +/- 8 and 296 +/- 65 (mean +/- S.E.), respectively.

Animals↗
PubMed1981

Crucial role of thyroid hormone in x-ray-induced neoplastic transformation in cell culture.

Incubation of mouse embryo fibroblasts (C3H/10T1/2) in media depleted of thyroid hormone for 1 week rendered the cells completely resistant to the transforming action of an x-ray dose, 4 grays, that yields transformation frequencies (no. foci per surviving cells) of approximately 10(-3) in media supplemented with triiodothyronine (T3) (1 nM). Studies on the timing of the additions or removal of the hormone indicate that T3 was maximally effective when added 12 hr before irradiation and that progression from the time of irradiation to the appearance of foci (6 weeks) was independent of the presence or absence of the hormone. The dependence of x-ray-induced transformation on the concentration of T3 in the medium was virtually the same as that for augmentation of Na+,K+-ATPase activity. The latter effect was used as a measure of T3 induction of protein synthesis. A further indication of the involvement of protein synthesis in the process is the abolition of T3- and x-ray-dependent transformation by cycloheximide at a concentration (100 ng/ml) that inhibits 50% of protein synthesis. We propose that thyroid hormone induces the synthesis of a host protein that is an obligatory participant in x-ray-mediated transformation.

Animals↗
PubMed1985

Neoplastic transformation in cell cultures: in-vitro/in-vivo correlations.

The behaviour of the C3H 10T1/2 C18 (10T1/2) cell line is reviewed in the context of its ability to reflect accurately events known to occur during carcinogenesis in vivo. It is concluded that, despite their embryonic fibroblastic origin and their infinite life-span in culture, 10T1/2 cells are capable of a wide range of responses to carcinogens and modulators of carcinogenesis that correspond closely to those observed in vivo, for the most part in epithelial tissues. For this and other reasons the 10T1/2 cell line has been widely employed in cancer research.

Animals↗
PubMed1982

Methionine regulation of N-5-methyltetrahydrofolate: homocysteine methyltransferase and its influence on the growth and protein synthesis in normal, neoplastic, and transformed cells in culture.

Normal human embryonic fibroblasts (CLV-58) and normal embryonic rat fibroblasts (REF) revealed equal growth in media containing 0.2 mM DL-homocysteine thiolactone (HOM) or in methionine (METH) enriched with 1.5 microM cyanocobalamin and 0.1 mM folic acid, whereas L 5178Y lymphoblasts and transformed rat fibroblasts (REF-S) showed more or less acute need for exogenous METH. In normal cells general protein synthesis remained unimpaired during 24 hours after substitution of METH by HOM. In L 5178Y and REF-S cells, however, protein synthesis was significantly inhibited. Measurements of N-5-methyltetrahydrofolate:homocysteine methyltransferase revealed a two- to threefold increase of enzyme activity in normal cells grown on HOM and in L 5178Y and REF-S cells grown on HOM with added METH. HeLa cells showed variability in growth pattern, in general protein synthesis response, and in inducibility of methyltransferase upon substitution of METH by HOM.

Animals↗
PubMed1980

The differential effect of normal cells and their neoplastic transformants on embryonic cell adhesion.

The adhesion of 7 day old embryonic chick neural retina cells was reduced by adult calf serum whereas foetal calf serum diminished adhesion to a lesser extent. Conditioned media from normal cells either increased the adhesion of neural retina cells or had no effect. Media from malignant cells reduced the adhesion of the retina cells. The results are discussed in relation to malignant invasion.

Animals↗
PubMed1988

[Transformation of rat esophageal precancerous epithelial cells and its biologic characteristics--establishment of RE25-3 esophageal carcinoma cell line].

A neoplastic transformation cell line (RE25-3) of the rat esophageal precancerous epithelium has been established by in vivo-in vitro method in our laboratory. Ten criteria were used to study the biological characteristics of the neoplastic transformation during various stages: 1. Dysplastic lesion of the esophageal epithelium was induced in wistar rat by oral administration of NSEE. The dysplastic epithelium was then removed and cultured. After several generations of subculture without carcinogen, the dysplastic epithelium showed neoplastic transformation in vitro. 2. The maximum mitotic index of the transformed cell reached 2.0% and two peaks were observed at hour 41 and 96, respectively, while the mitotic index of the normal esophageal cell was 0.6%. 3. DNA measurement was performed by MSP. The results showed disappearance of the diploid cell from the fifth subculture. Tetraploid, heteroploid and aneuploid cells were observed from the third subculture. The aneuploid cells amounted to 86.24%. 4. The number of chromosome increased as the time of culture as well as the number of subculture generation increased. Chromosome aberration was observed. 5. As the number of subculture generation increased, the damage and break of the chromosome increased. Micronuclei rate increased. 6. By incorporation of H3-TdR, DNA synthesis rate increased as the malignancy increased. 7. Growth of the RE25-3 cell was dependent on EGF in the early stage. But after 15 subculture, as neoplastic transformation developed, this dependency disappeared. 8. After 14 generations of subculture, the cell can be cultured in soft ager. 9. Keratin was proved positive within the cell by ABC immuno-histochemistry assay.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Marker chromosome stability associated with neoplastic transformation of human uroepithelial cells.

Chromosome studies were performed on three independently derived tumor cell lines established from carcinomas induced in nude mice after innoculation of SV40 immortalized human uroepithelial cells that had been treated with methylcholanthrene. Tumor 1 was an undifferentiated carcinoma, while tumors 7 and 9 were both squamous carcinomas. After six to eight passages in vitro the tumor cells were each reinoculated into other nude mice to yield secondary tumors (1.1 and 7.1). Chromosome studies on both primary and secondary tumors demonstrated the same distinctive chromosome markers. Tumors 1 and 1.1 shared the same histopathology in addition to the same modal chromosome number and identical chromosomal duplications and deficiencies; the same was true of tumors 7 and 7.1. Tumor 9, which did not yield a secondary tumor, nevertheless showed the same chromosome pattern in different passages. The stability of the characteristic marker chromosomes in the three tumor cell lines distinguishes these malignant lines from the nonmalignant SV40 transformed parent line from which the three tumors derived because the parent line was characterized by extreme marker instability. This suggests that the stable marker chromosomes that characterize the tumor cell lines may be critical for their tumorigenicity, and that evolution of an adaptive neoplastic genome may select for cytogenetic stability as long as there are no new selective pressures.

Animals↗
PubMed1982

[2 malignant cell lines derived from strain L6 of rat myogenic cells].

A nonfusing variant M4 of the L6 line of rat myoblasts was isolated. This subline was tumorigenic when inoculated into suckling rats. Comparative studies of cells growth in vitro, serum requirement, cell adhesiveness and capacity to form colonies in soft agar confirmed that M4 cells had undergone neoplastic transformation while L6 cells exhibited normal characteristics. Another subline designated as RMS4 was derivated from M4 cells tumors. Growth characteristics in vitro and karyotype analysis indicated that RMS4 cells presented a higher degree of transformation as compared with M4 cells. Both M4 and RMS4 cell cultures seem to produce a C-type virus.

Animals↗