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PubMed1984

[Tumorigenicity of the cell lines (TTK-1 cell lines) derived from normal human decidua in nude mice].

Two cell lines, TTK-1(E) and TTK-1(F), derived from normal human early decidual tissue have been maintained in culture through forty subcultures since July, 1979. These cell lines were transplanted subcutaneously into nude mice at 6 weeks of age to investigate their tumorigenicity. Rapidly growing tumor nodules formed at the site of implantation. The incidence of tumor growth was 60% in TTK-1(E) and 80% in TTK-1(F). The tumor tissues were composed of poorly differentiated cells arranged in cord-like and/or gland-like structures, and showed the malignant histological characteristics. Light microscopic and electron microscopic studies revealed that the properties of the tumor cell populations are identical with those of the culture cells of the two cell lines before implantation. These results obviously indicated that the tumors had grown from the implanted cells. Although the tumors developed from the respective two cell line showed some common histological features, they apparently differed in light microscopic and electron microscopic findings. Tumorigenesis with malignant features could be attributed to the in vitro spontaneous neoplastic transformations during successive subcultures, which might be useful as an in vitro model of endometrial carcinogenesis.

Adenocarcinoma↗

PubMed2001

In vitro uptake of polystyrene microspheres: effect of particle size, cell line and cell density.

Uptake of polycation-DNA particles is the first step in achieving gene delivery with non-viral vehicles. One of the important characteristics determining uptake of DNA particles is their size. Here we have characterized the ability of several cell lines to internalise labelled polystyrene microspheres of different sizes. All the cell lines tested ingested 20-nm microspheres avidly. With larger microspheres (93, 220, 560 and 1010 nm) cell type as well as growth related differences were observed. Whereas some cell lines (HUVEC, ECV 304 and HNX 14C) took up microspheres up to 1010 nm even when the cells were confluent, others did not take up many microspheres larger than 93 nm (Hepa 1-6 and HepG2). In one cell line (KLN 205), uptake of 93-, 220- and 560-nm microspheres was avid in growing cells, but not detectable when they were confluent. In KLN 205 cells, a good correlation was found between the uptake of 560-nm microspheres and the uptake of a peptide-DNA polyplex formulation, when it was prepared under conditions leading to small particle sizes. Little correlation was found when the polyplex formulation was allowed to aggregate.

Amino Acid Sequence↗

PubMed1993

Transient expression of the Epstein-Barr virus LMP1 gene in B-cell chronic lymphocytic leukemia cells, T cells, and hematopoietic cell lines: cell-type-independent-induction of CD23, CD21, and ICAM-1.

The Epstein-Barr virus (EBV) genome has recently been detected in various non-B cell neoplasms, including various T-cell leukemias and in Reed-Sternberg cells of Hodgkin's disease, but the contribution of EBV genes to the transformed phenotype remains unclear. We have investigated the possible effect which the EBV genes LMP1 and EBNA2, of which the expression has been reported in non-B cell neoplasms, may have on a variety of cell types. The LMP1 and EBNA2 genes were transiently expressed from heterologous promoters in two human T-cell lines (HPB-ALL and Jurkat), two human cell lines of the myeloid lineage (K562 and U937), one type I Burkitt's lymphoma cell line (Rael) and in human primary T cells and B-cell chronic lymphocytic leukemia cells. The cell surface expression of CD23, CD21, ICAM-1 and LFA-1 was monitored on transfected cells. In the cell lines, except U937, the surface antigens CD21 and ICAM-1 were upregulated in a dose-dependent and transient manner by the transient expression of LMP1, and EBNA2 slightly enhanced the effects of LMP1 on CD23 and CD21 upregulation. LMP1 also induced increased CD21, ICAM-1 and LFA-1 surface expression on transfected primary T-cells, and CD21 and ICAM-1 in four of five B-cell chronic lymphocytic leukemias tested. Finally, LMP1 transient expression caused increased cell size of the primary T cells and responding B-cell chronic lymphocytic leukemia cells. Our results strongly suggest that LMP1 can trigger specific responses in a variety of white cell types and thus is probably contributing to the phenotype of EBV-positive tumor cells not only in the B-cell lineage.

Antigens, Viral↗

PubMed1991

In vitro enhancement of cis-platinum antitumor activity by caffeine and pentoxifylline in a human ovarian cell line.

Cell kinetic perturbations measuring DNA and nuclear protein with dual-parameter flow cytometry were studied in vitro after cis-platinum (DDP) treatment of a DDP-resistant human ovarian cell line (BG-1). Cell viability (trypan blue exclusion) and the cell's ability to replicate (replicating potential) are also reported. A dose-dependent G2 arrest and concomitant increase in cytotoxicity were observed. We also observed a marked increase in cytotoxicity of 2.5 micrograms/ml DDP with the addition of 1 mM of caffeine (CAF) or pentoxifylline (PTX). Additionally, the cells treated with DDP and CAF or DDP and PTX demonstrated a markedly diminished ability to replicate. Cell cycle perturbations, especially the G2-phase arrest, were markedly enhanced in the cells treated with DDP and CAF or DDP and PTX, when compared to that in cells treated with DDP alone. We conclude that the cytotoxicity of DDP is enhanced by CAF and PTX in vitro by inhibiting DNA repair during the S and G2 phases.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1992

Expression and involvement of c-fos and c-jun protooncogenes in programmed cell death induced by growth factor deprivation in lymphoid cell lines.

Cell death induced by growth factor withdrawal is a programed event in which gene transcription and translation are required. Thus, it is likely that genes encoding for transcriptional factors can play an important role in this process. We have tested this hypothesis by analyzing c-fos and c-jun protooncogene expression and involvement in lymphoid cells deprived of growth factors. Interleukin (IL)-6- and IL-2-dependent mouse cell lines undergo programmed cell death after growth factor deprivation. Northern blot analysis shows that c-fos and c-jun protooncogenes are rapidly induced (within 60 min) after growth factor deprivation in IL-6- and IL-2-dependent mouse cells. Induction is transient, being undetectable at 120 min after deprivation. Induction of these protooncogenes is at the transcriptional level, as demonstrated by actinomycin D and nuclear run-off experiments. Antisense oligonucleotides directed against c-fos and c-jun mRNAs consistently reduced the expression of these genes in treated cells. This reduction was associated with increased survival of growth factor-deprived lymphoid cells, thus suggesting that the expression of c-fos and c-jun protooncogenes may represent an important early event in the activation of the genetic program of cell death.

Base Sequence↗

PubMed1998

Differential expression of cytokine transcripts in human epithelial ovarian carcinoma by solid tumour specimens, peritoneal exudate cells containing tumour, tumour-infiltrating lymphocyte (TIL)-derived T cell lines and established tumour cell lines.

T cell lines derived in low concentrations of recombinant IL-2 (rIL-2) from TIL of patients with epithelial ovarian carcinoma (EOC) often exhibit specific cytotoxicity against autologous tumour cells. However, the ability of T cells at the tumour site to respond to ovarian carcinoma cells may be affected by the production of cytokines by the various cell types present. Using reverse transcriptase-polymerase chain reaction (RT-PCR) we investigated cytokine transcripts in: (i) established EOC tumour cell lines; (ii) solid tumour specimens or peritoneal exudate cells (PEC) from ascites or peritoneal washings of patients with EOC; and (iii) CD4+ TCRalphabeta+ and CD8+ TCRalphabeta+ TIL-derived T cell lines developed in rIL-2. We have found that (i) established EOC tumour cell lines expressed transcripts for transforming growth factor-beta 2 (TGF-beta2) (7/7), but not IL-10 (0/7) or interferon-gamma (IFN-gamma) (0/7) and rarely IL-2 (1/7); (ii) PEC expressed transcripts for IL-2 (12/13), IL-10 (9/13), and TGF-beta2 (12/13), and less often, IFN-gamma (3/13), whereas solid tumour specimens from eight patients with EOC expressed transcripts for IL-2 (4/8), TGF-beta2 (4/8), and IL-10 (5/8), but not for IFN-gamma (0/8); (iii) CD4+ TCRalphabeta+ T cell lines expressed transcripts for IFN-gamma (4/4), IL-2 (4/4) and IL-10 (3/4), whereas CD8+ TCRalphabeta+ T cell lines expressed transcripts for IFN-gamma (5/5), IL-2 (1/5) and IL-10 (2/5). None of these T cell lines expressed TGF-beta2 transcripts. The frequency of IL-2 and TGF-beta2 transcripts in solid tumours was significantly lower than in the PEC (P = 0.0475). CD4+ or CD8+ T cell lines expressing IFN-gamma, IL-2 and IL-10 transcripts were derived in culture with rIL-2 from the TIL of specimens that did not necessarily express these cytokines in the absence of rIL-2. The frequency of cytokine transcripts in T cell lines compared with these same transcripts in the PEC was significantly higher for IFN-gamma (P = 0.0005) and lower for TGF-beta2 (P = 0.0001). An association was observed between the expression of cytokine transcripts in vivo or by TIL-derived cell lines and functions exhibited by either production of cytokines or in vitro cytotoxicity.

Adenocarcinoma↗

PubMed1990

Evidence for deficiency of low density lipoprotein receptor on human colonic carcinoma cell lines.

Cells from six human colonic adenocarcinoma lines (CaCo-2, HT29, LS174T, SW480, SW403, and SW1417) and a normal skin fibroblast cell line (AG1519) were assayed in vitro for their ability to use low density lipoprotein (LDL). All tumor cell lines grew well in lipoprotein-deficient serum, implying that LDL in culture medium was not critical for cell growth. When cell growth was inhibited with mevinolin, a cholesterol synthesis inhibitor, the addition of LDL to the medium had no effect on the growth of cells from five of six tumor cell lines. CaCo-2 cells showed a moderate reversal while the fibroblast control showed total reversal of inhibition. A monoclonal antibody to bovine/human LDL receptor, used in an enzyme-linked immunosorbent assay, indicated that only CaCo-2 cells and human skin fibroblast cells consistently demonstrated the presence of LDL receptors. Thus, five of six colon tumor cell lines were unable to overcome a mevinolin block in cholesterol metabolism indicating that these cells were deficient in LDL receptors.

Antibodies, Monoclonal↗

PubMed1976

Cell cycle and morphological changes during growth and differentiation of a rat basophilic leukemia cell line.

Cells of the rat basophilic leukemia cell line RBL-1 differentiated maximally when permitted to achieve growth arrest in a high-density stationary phase, in which the cell number is constant, and the cells are arrested in a G phase of the cycle. Features of differentiation are the accumulation of large basophilic granules and increases in membrane receptors for immunoglobulin E. However, changes in histamine content did not parallel granule development or changes in immunoglobulin receptor concentration. During rapid "forced exponential" growth, the cell number doubles every 8 hr, 50% of the cells are in S phase, and differentiation is minimal.

Animals↗

PubMed1988

Comparative human cellular radiosensitivity: II. The survival following gamma-irradiation of unstimulated (G0) T-lymphocytes, T-lymphocyte lines, lymphoblastoid cell lines and fibroblasts from normal donors, from ataxia-telangiectasia patients and from ataxia-telangiectasia heterozygotes.

We have measured clonal survival following gamma-irradiation of unstimulated (G0) T-lymphocytes from 35 donors, of 11 T-lymphocyte cell lines, of six lymphoblastoid cell lines, and of nine primary fibroblast strains for which we have G0 T-lymphocyte material from the same donor. Amongst the G0 lymphocytes we have results from nine normal donors, from eight cord bloods, from seven ataxia-telangiectasia (A-T) patients and from nine A-T heterozygotes. Although there is some variation between samples, G0 T-lymphocytes from normal donors appear to be slightly more radioresistant than T-lymphocyte lines, with a more shouldered survival curve. From our limited sample, lymphoblastoid cell lines appear to be slightly more radiosensitive than T-lymphocytes. The overall radiosensitivity of primary fibroblasts appears to be broadly similar to that of G0 T-lymphocytes. In nine instances, five A-Ts and four A-T heterozygotes, both G0 T-lymphocytes and primary fibroblasts from the same donor were tested. In five cases there was closely similar radiosensitivity in the two cell types, but in four cases there was some discrepancy. Further work, especially with normal donors, will be required in order to establish how reliably radiosensitivity in other cell types can be predicted from that of G0 T-lymphocytes. In all cell types the hypersensitivity of A-T cells was confirmed. Furthermore, the marginally greater sensitivity of A-T heterozygotes, when compared as a group with normals, was confirmed with G0 T-lymphocytes. Our results also suggest a slightly increased radiosensitivity in G0 T-lymphocytes from some, but not all, cord blood samples.

Ataxia Telangiectasia↗

PubMed1998

Development of engineered pancreatic beta-cell lines for cell therapy of diabetes.

Insulin-secreting pancreatic beta-cell lines represent a promising approach for treatment of insulin-dependent diabetes mellitus (IDDM). Our laboratory has developed a number of highly-differentiated beta-cell lines in transgenic mice. These cells produce insulin amounts comparable to normal pancreatic islets and release it in response to physiological insulin secretagogues. Using a reversible transformation system it has become possible to tightly regulate cell replication in these beta-cell lines both in culture and in vivo. By employing adenovirus genes which downreguate antigen presentation and increase cell resistance to cytokines mouse beta cells could be transplanted across allogeneic barriers. These approaches could be applied to the development of human beta-cell lines by genetic engineering of isolated human islets.

Journal Article↗

PubMed1998

Expression of HLA class I antigens in transporter associated with antigen processing (TAP)-deficient mutant cell lines.

Cells lacking expression of the transporter associated with antigen processing (TAP) are deficient in surface HLA class I, yet express reduced levels of HLA-A2 antigen through TAP-independent processing pathways. We have analysed the expression of HLA-A, -B and -C antigens on the 721.174 and T2 TAP-deficient mutant cell lines using a panel of monoclonal antibodies specific for the HLA antigens encoded by the genotype of these cells. Our study has shown the constitutive expression of HLA-Cw1 molecules on the cell surface of both T2 and 721.174 cells and has confirmed that HLA-A2 and HLA-B51 are expressed at low levels. Transfection of 721.174 cells with cDNAs encoding TAP1 and TAP2 proteins did not fully restore HLA class I antigen expression on these cells, which appeared to be mainly due to a deficiency in expression of the HLA-B51-associated Bw4 epitope. This suggests that additional antigen-processing genes may be required for optimal generation of HLA-B-binding peptides. Our results indicate that TAP-independent pathways of antigen-processing provide peptides for functional expression of all three classical HLA class I molecules.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed1998

Insulin receptor substrate 1 antisense expression in an hepatoma cell line reduces cell proliferation and induces overexpression of the Src homology 2 domain and collagen protein (SHC).

In mammalian cells, the insulin receptor substrate 1 protein (IRS-1) is a specific substrate for insulin and IGF-1 receptor tyrosine kinases which is involved in mediating metabolic and mitogenic actions of insulin and IGFs. In order to determine if IRS-1 is also essential in a chicken derived hepatoma cell line (LMH cells), IRS-1 gene has been invalidated in these cells. For this, we subcloned chicken IRS-1 gene in an antisense orientation into a mammalian expression vector driven by the cytomegalovirus early promoter. LMH cells were stably transfected with this construct or with the empty vector carrying only the neomycin resistance gene and selected for cIRS-1 expression. One subclone, C2, showed a complete repression of cIRS-1 expression at both protein and mRNA levels. Proliferation of C2 cells was dramatically reduced (54%) compared with Neo(r) cells. Furthermore this reduction was accompanied by a decrease in insulin-dependent [3H]thymidine incorporation, indicating a reduction in DNA synthesis. Insulin-dependent [U-14C]glucose incorporation into cellular lipids was also significantly reduced in C2 cell line suggesting an alteration in lipogenesis. In wild type LMH cells, SHC which is involved in Ras pathway, also served as a substrate for insulin receptor tyrosine kinase. In C2 cells, SHC expression, its association with the insulin receptor and its tyrosine phosphorylation were largely increased. Two forms of the regulatory subunit of PI 3-kinase were present: p85 and p55 forms. Furthermore, C2 cells displayed increased basal phosphatidylinositol (PI) 3'-kinase activity. This report demonstrates a role for cIRS-1 in the metabolic and mitogenic actions of insulin in LMH cells. However, the overexpression of cIRS-1 antisense did not completely abolish cell proliferation. This may be explained by the exacerbation of an alternative pathway that only partly compensate for the knocking out of cIRS-1 gene: the overexpression of SHC.

Adaptor Proteins, Signal Transducing↗

PubMed2001

SeO(2) induces apoptosis with down-regulation of Bcl-2 and up-regulation of P53 expression in both immortal human hepatic cell line and hepatoma cell line.

An immortal human hepatic cell line HL-7702 and human hepatoma cell line SMMC-7721 were treated with 3-30 microM SeO(2). SeO(2) at 30 microM markedly inhibited cell proliferation and viability, and prompted apoptosis of both normal hepatic and hepatoma cells after 48h treatment. SeO(2) could also down-regulate the Bcl-2 level, greatly in HL-7702 and slightly in SMMC-7721 cells, but up-regulate wild type P53 level a little in HL-7702 and significantly in SMMC-7721 cells. The Bcl-2/P53 value was closely correlated with the apoptotic rate as well as SeO(2) concentrations.

Apoptosis↗

PubMed1997

Normal FHIT transcripts in renal cell cancer- and lung cancer-derived cell lines, including a cell line with a homozygous deletion in the FRA3B region.

The recently identified FHIT gene encompasses the FRA3B region and the breakpoint of a constitutive t(3;8) occurring in a family with hereditary renal cell cancer. Occurrence of aberrant transcripts in different types of tumours has led to the suggestion that FHIT might play a critical role in the development of various types of cancer. We have analyzed the gene and its transcripts in lung cancers and renal cell cancer-derived cell lines. A lung adenocarcinoma cell line, GLC-A2, appeared to have a homozygous deletion in intron 5 of FHIT. RT-PCR analysis revealed a normal-sized PCR product in all of the cell lines: Including GLC-A2. A number of them had an additional aberrant product. Analysis of a great number of control cell lines and tissues showed that the majority of these also had aberrant PCR products in addition to a normal-sized PCR product. Different specimens of the same cell type showed variable additional RT-PCR products. Normal-sized PCR products had a sequence identical to the FHIT sequence. PCR products longer than normal had insertions of different sizes at different positions. With three exceptions, PCR products shorter than normal represented FHIT sequences missing one or more entire exons. Thus, the presence of aberrant transcripts is not cancer-specific. Conceivably, sequence responsible for the instability of the FRA3B region are being transcribed into FHIT pre-mRNA and may cause the abnormal splicing and processing of the transcripts.

Acid Anhydride Hydrolases↗

PubMed2000

Different responses to acute or progressive osmolarity increases in the mIMCD3 cell line.

Cells from the kidney medulla are able to survive and function when exposed to high concentrations of NaCl and urea. In vitro, cultured epithelial cells from the kidney medulla are able to survive stronger acute hyperosmotic shocks when both solutes are present. However, in vivo, increases in osmolarity are not acute. In this study, we compared the survival of a murine renal epithelial cell line during acute or progressive (two step) adaptation to hypertonic NaCl and/or urea. Increasing osmolarity to 700 mOsm/l with NaCl or urea in a single step led to massive cell death ( 50% in 24 hours). However, genomic DNA of dying cells was not degraded, and electron microscopy revealed weak condensation of chromatin, absence of membrane blebbing, and no nuclear indentation. Pre-adaptation to permissive concentrations of NaCl (200 mOsm/l giving a final osmolarity of 500 mOsm/l) protected cells against subsequent increases in osmolarity, allowing adaptation to final osmolarities as high as 900 mOsm/l. In contrast, pre-adaptation to permissive concentrations of urea (200 mOsm/l) did not lead to enhanced cell survival after a subsequent 200 mOsm/l step. Cell death was as rapid as after an acute shock, but was more typical of apoptosis (genomic DNA laddering, strong chromatin condensation, nuclear indentation, and blebbing of the membrane giving rise to apoptotic bodies). Thus, acute hyperosmolarity induces cell death with essentially similar responses to NaCl and urea. In contrast, progressive adaptation of mIMCD3 cells to NaCl allows cell survival, whereas progressive adaptation to hyperosmotic urea triggers a cell death pathway different from the one triggered by acute hyperosmotic shocks.

Adaptation, Physiological↗

PubMed1984

[Cultivation of the transmissible gastroenteritis virus in a continuous cell line].

Cell cultures of the permanent cell line SPEV to which the transmissive gastroenteritis virus had already been adapted were used to culture the virus and carry out the virus-neutralization test. Use was made of a cell suspension of a variable density--300 and 500 thou cells per cm3. Both variants of the cell suspension were comparatively studied in terms of growth, the production of a monolayer, susceptibility to infection, and titer of the virus obtained, using 4 test tubes with the virus at various rates of dilution which were kept under observation daily, keeping a record of the infected and noninfected cell cultures. The amount of the virus was determined by titration. It was found that the monolayer was produced more rapidly in the suspension containing 500 thou cells/cm3. In that case infection could be performed at the 24th hour. The cytopathic effect was more pronounced, and the titer of the virus obtained was higher. Successful attempts were made with the virus-neutralization test with the infection of the cell cultures in suspension. Thus, the entire procedure was shown to be labour-saving as the time for investigation of the sera was shortened.

Animals↗

PubMed1983

Esterification of monohydroxyfatty acids into the lipids of a macrophage cell line.

Cells of a mouse macrophage-like tumor cell line, J774.2, were incubated with 0.6 microM radiolabeled mono- and di-hydroxyfatty acids. Monohydroxyfatty acid products of the neutrophil and platelet lipoxygenase pathways (5-HETE, 15-HETE, and 12-HETE) were rapidly taken up (42-64% of the counts cell associated at 1 min) and esterified into triglycerides and phospholipids. 5-HETE and 12-HETE were found in triglycerides and distributed among phospholipid classes while 50% of added 15-HETE was esterified into phosphatidyl inositol. Treatment of phospholipids from cells incubated with 5-HETE, 12-HETE, and 15-HETE with phospholipase A2 resulted in release of the respective monohydroxyfatty acid. HHT, a monohydroxyfatty acid product of the cyclooxygenase pathway, was taken up and esterified more slowly than the lipoxygenase products. In addition, HHT was not released when the phospholipids from cells incubated with HHT were treated with phospholipase A2. LTB4, a dihydroxyfatty acid product of neutrophil lipoxygenase, was not taken up by J774.2 cells. The unique patterns of uptake and intracellular distribution of the different monohydroxyfatty acids suggests that the enzymes involved in the esterification of these compounds have substrate specificity and may also relate to the specific biologic effects of these compounds.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

PubMed1999

Activation of integrin and ceramide signalling pathways can inhibit the mitogenic effect of insulin-like growth factor I (IGF-I) in human breast cancer cell lines.

Cell counting, cell cycle analysis and Western immunoblotting were used to examine the effects of non-apoptotic doses of a ceramide analogue, C2, and a synthetic arginine-glycine-aspartic acid (RGD)-containing peptide, RGD, in MCF-7 and T47D cells to determine whether activation of these signalling pathways could alter the mitogenic potential of insulin-like growth factor I (IGF-I). IGF-I alone increased total cell number in both cell lines, associated with a rise in the percentage of cells in the S-phase of the cell cycle and a co-incident increase in cyclin A production. Treatments alone had no effects on cell number or cyclin A production relative to controls. C2 inhibited IGF-I-induced mitogenesis in both lines, whereas RGD was only effective in the T47D line. Despite inhibition of cell proliferation, IGF-I stimulation of cells in S-phase and of cyclin A levels were unaffected; however, an IGF-I-induced increase in cyclin B1 levels was inhibited by 30%. Low-dose induction of integrin and ceramide signalling pathways causes cells to be blocked in S-phase, thereby inhibiting the normal cycle of events associated with the IGF-I-induced mitotic signal. Activating these pathways may not only restrict tumour growth by induction of apoptosis but they may also directly inhibit IGF-I-induced cell proliferation.

Breast Neoplasms↗