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Results for “Cell Line, Tumor”

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At least 19 recordsLinked to original sources

PubMed1987

Interferon-gamma, interferon-alpha/beta, and tumor necrosis factor differentially affect major histocompatibility complex class I expression in murine leukemia virus-induced tumor cell lines.

Tumor cell lines induced by Gross murine leukemia virus were examined for cell-surface major histocompatibility complex class I expression. Three of five cell lines constitutively express H-2K and H-2D class I protein. Culturing these cells with interferon (IFN)-gamma, IFN-alpha/beta, or tumor necrosis factor increases both K and D expression in these cell lines. Two of five tumor cell lines express no class I proteins by fluorescence-activated cell sorter analysis, specific immunoprecipitation, and specific hybridization in Northern analysis. Treatment with IFN-gamma induces D, but not K protein expression in one of these cell lines. IFN-alpha/beta and tumor necrosis factor induce neither D nor K expression in this cell line. Thus, these two cytokines appear to have different mechanisms of action than IFN-gamma for altering class I expression. The other class I-negative tumor cell line does not express either K or D proteins under any conditions tested. All five cell lines express beta 2-microglobulin; this expression is increased by IFN-gamma treatment even in cell lines which do not express class I heavy chain. The results of this study demonstrate that 1) different tumor cell lines demonstrate variations in class I gene regulation, and 2) differences in regulation between class I genes may occur within a single cell line.

AKR murine leukemia virus↗

PubMed1990

[An efficient method for establishing murine tumor cell lines].

Tumor cells were cultured in RPMI1640 medium with 16% fetal calf serum and 5% conditioned medium of PHA-stimulated murine spleen cells. After cloning, the tumor cells were reinoculated into normal susceptible mouse. When tumor developed, they grew easily in subsequent cultures in vitro, thus establishing tumor cell lines. By this method, 5 leukemia cell lines and 2 tumor cell lines have been established.

Animals↗

PubMed1998

Down-regulation of the transporter for antigen presentation, proteasome subunits, and class I major histocompatibility complex in tumor cell lines.

Tumor cells may alter the expression of proteins involved in antigen processing and presentation, allowing them to avoid recognition and elimination by cytotoxic T cells. In this study, reverse transcription-PCR was used to assess the expression in human tumor cell lines of mRNA for multiple components of the class I MHC antigen-processing pathway, including several proteasome subunits that have been implicated in antigen processing but have not been previously examined in this context (e.g., low molecular weight polypeptide proteasome subunit (LMP) 10, proteasome activator (PA) 28alpha, and PA28beta). Deficiencies in the expression of antigen-processing genes were demonstrated in 9 of 27 cell lines, representing a variety of histological types. In some cases, virtually complete deficiencies were observed in the expression of the four genes encoded within the MHC (TAP1, TAP2, LMP2, and LMP7), as well as LMP10, which is encoded outside the MHC. Combined deficiencies of these gene products were common, and marked deficiency of LMP10 was found in five of the nine cell lines with deficits. The existence of deficiencies in the expression of genes at dispersed loci suggested that the basis for the deficiencies was a regulatory mechanism, as opposed to mutation or deletion of these genes. Furthermore, most of the deficiencies were reversed by treatment with IFN-gamma. In contrast to such extreme deficiencies, we found unaltered or only partially decreased expression of PA28alpha and PA28beta in tumor cell lines. Thus, tumors may evade immune surveillance by simultaneously down-regulating multiple components of the MHC-I antigen-processing pathway, thereby altering the processing and presentation of tumor antigens. Expression of essential proteasome subunits, however, may still be maintained.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed1981

Episomal and nonepisomal herpesvirus DNA in lymphoid tumor cell lines.

Tumor cell lines derived from Herpesvirus saimiri (H. saimiri)- and Herpesvirus ateles (H. ateles)-induced lymphomas of New World primates and rabbits contain multiple copies of viral genomes. Partial denaturation mapping and blot hybridizations of episomal DNA from lymphoid tumor cell line No. 1670 showed that a 12.5md-fragment is missing which represents the EcoRI D- and H-fragments of virion L-DNA. However, the missing piece can be demonstrated in total cellular DNA by reassociation kinetics, possibly because it persists in integrated form. Both episomal and nonepisomal H-DNA are heavily methylated in a number of the lymphoid cell lines, and methylation may be reduced by conventional methylation inhibitors (S-adenosyl homocystein, SIBA) as well as by the tumor promoting phorbol ester TPA.

Animals↗

PubMed1990

Platelet derived growth factor (PDGF) autocrine components in human tumor cell lines.

Tumor cells may stimulate their own proliferation through an autocrine mechanism by simultaneously producing growth factors and growth factor receptors. We now report that numerous human tumor-derived cell lines simultaneously express the genes for platelet-derived growth factor (PDGF) A and B chains and the PDGF receptor (PDGF-R). Measurement of mRNA transcribed from these genes showed that among 16 malignant glioma cell lines tested, 15 expressed the PDGF A gene, 12 expressed the PDGF B gene, and 13 expressed the PDGF-R gene. Of three osteosarcoma lines, three expressed PDGF A, two expressed PDGF B, and three expressed PDGF-R. For eight malignant melanoma lines, seven expressed PDGF A, five expressed PDGF B, and three expressed PDGF-R genes. Thus, 13 of 16 malignant glioma, 3 of 3 osteosarcomas, and 3 of 8 malignant melanoma cell lines expressed the PDGF receptor gene and either or both PDGF genes. Five cell lines were tested for production of biologically active PDGF and PDGF receptor protein. Media conditioned by each of the five cell lines induced tyrosine phosphorylation of a protein identical in size to the PDGF receptor. These five cell lines also produced PDGF receptor protein as measured by Western blot analysis or metabolic labeling and immunoprecipitation using PDGF-R antibodies. The PDGF receptors of these cell lines were activated by human platelet PDGF or by recombinant AA or BB homodimers. Intracellular interaction of these receptors with the growth factor simultaneously produced may provide continuous stimulation to the proliferation of these cells.

Animals↗

PubMed1986

Endemic Burkitt's lymphoma: phenotypic analysis of tumor biopsy cells and of derived tumor cell lines.

Tumor cells from 10 patients with Epstein-Barr virus-positive endemic Burkitt's lymphoma (BL) have been examined for cell surface phenotype, both at the biopsy stage and during BL cell line outgrowth in vitro, the cultures being followed for up to 150 passages. In all 10 cases, the biopsy cells showed coexpression of the common acute lymphoblastic leukemia antigen (CALLA) and of the BL-associated glycolipid antigen (BLA) with no accompanying expression of several "lymphoblastoid" cell surface markers defined by selected monoclonal antibodies. During cell line establishment and in vitro passage, the individual BL cell lines showed different degrees of progression toward a more "lymphoblastoid" cell surface phenotype, some even losing CALLA and BLA expression while retaining the chromosomal translocations indicative of their malignant origin. This differential capacity for phenotypic progression in vitro explains much, if not all, of the heterogeneity of the BL cell phenotype apparent from many previous studies with panels of long-established lines. Such heterogeneity in vitro belies the true homogeneity of the tumor cell phenotype in vivo.

Antibodies, Monoclonal↗

PubMed2000

[Somatostatin receptor subtype 2 mRNA expression in human gastric immortalized cell line and tumor cell lines].

OBJECTIVE: Inhibition of somatostatin on cell proliferation via somatostatin receptor subtype 2 (SS-R2), suggested this receptor subtype may be involved in tumor growth. Present study is to demonstrate whether SS-R2 was expressed in tumor cell lines extensively as well as in human gastric epithelia immortalized cell line. Meanwhile, the effect of p53 mutation on SS-R2 expression in gastric cancer cell line was also elucidated. METHODS: Full-length human somatostatin receptor subtype 2 cDNA was cloned by RT-PCR. Using cDNA as the probe and RT-PCR, expression of mRNA for SS-R2 in 9 cancer cell lines and human gastric immortalized cell line was detected. RESULTS: Data revealed that most cancer cell lines but a pancreatic cancer cell line expressed SS-R2 mRNA. CONCLUSION: Regardless whether p53 mutation or not in human gastric cancer cell lines, SS-R2 mRNA was transcribed.

Cell Line↗

PubMed1990

The interaction between recombinant human tumor necrosis factor and radiation in 13 human tumor cell lines.

Tumor necrosis factor (TNF) was cytotoxic at concentrations of 10 to 1000 units/ml to 12 of 14 human tumor cell lines. Synergistic or additive cell killing between TNF and radiation was observed in 7 of 10 tumor cell lines, while independent tumor cell killing by each agent occurred in two tumor cell lines. The maximum synergistic effect was observed when TNF was added 4-12 hr prior to irradiation. This interaction was absent when TNF was added after irradiation. TNF also reduced potentially lethal damage repair in 3 of 5 cell lines tested. Possible mechanisms of interaction of TNF and X rays including induction of hydroxyl radicals and subsequent DNA damage by TNF and radiation are discussed.

Animals↗

PubMed1978

Karyotype analysis of a frog pronephric tumor cell line.

Pronephric tumor cell lines, established from explants of a herpes virus induced frog renal adenocarcinoma, were shown to have a aneuploid modal chromosome number of 39. A karyotypic analysis of one line demonstrated the presence of abnormal chromosomes and chromosomal aberrations not previously reported for Lucké tumor cells. The cell line was characterized by two marker chromosomes of high incidence, but there was no evidence of a stemline population of tumor cells.

Adenocarcinoma↗

PubMed1988

Tumor necrosis factor expression in human epithelial tumor cell lines.

Tumor necrosis factor (TNF) is a monokine with in vitro cytotoxicity for some but not all tumor cells. The basis for sensitivity and resistance to the antitumor effects of this agent remains unclear. The present studies have monitored the effects of TNF on 14 epithelial tumor cell lines. Eleven of these cell lines were resistant to the growth inhibitory effects of TNF (50% inhibitory concentration greater than 1,000 U/ml). 12 of the 14 tumor cell lines has detectable levels of high affinity cell surface TNF binding sites, thus suggesting that resistance was not often due to the absence of cell surface TNF receptors. Northern blot analysis demonstrated that three of the eleven resistant cell lines expressed detectable levels of TNF mRNA. Furthermore, both sensitive and resistant epithelial tumor cells had the capacity to express TNF transcripts in the presence of the protein synthesis inhibitor, cycloheximide. Finally, the presence of TNF expression at the RNA level is shown to be associated with the production of a TNF-like protein in the resistant Ov-D ovarian carcinoma cells. These findings suggest that certain human epithelial tumor cell lines inherently resistant to TNF also express this cytokine.

Animals↗

PubMed1995

CDKN2 (MTS1) tumor suppressor gene mutations in human tumor cell lines.

Tumor suppressor gene CDKN2 (also called MTS1, CDK4I and p16INK4) is located in 9p21 and deleted homozygously in a high percentage of tumor cell lines. We have examined the sequence of CDKN2 in 154 tumor cell lines that are not homozygously deleted for CDKN2. Overall, 18% (27/154) of the cell lines carried mutations in CDKN2. These mutations were found in cell lines derived from melanoma, bladder, lung and prostate cancers, as well as sarcomas of various origin. The spectrum of the CDKN2 mutations found in melanoma cell lines indicated a major role for ultraviolet light in generating the mutations, suggesting the mutations occurred in vivo. The frequency of loss of heterozygosity in 9p21 in this set of lines is only slightly higher than the background rate of aneuploidy, suggesting that a second 9p21 tumor suppressor gene, if it exists, must lie near CDKN2.

Amino Acid Sequence↗

PubMed1986

Transfection of DNA from a chloroethylnitrosourea-resistant tumor cell line (MER+) to a sensitive tumor cell line (MER-) results in a tumor cell line resistant to MNNG and CNU that has increased O-6-methylguanine-DNA methyltransferase levels and reduced levels of DNA interstrand crosslinking.

A subclone of a human glioma tumor cell strain which was deficient at O-6-alkylguanine repair was transfected with DNA from an O-6-alkylguanine DNA alkyltransferase-positive human colon tumor cell line (HT29). The transfected subclone, which was selected by its resistance to N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), acquired increased resistance to chloroethylnitrosourea (CNU), contained O-6-methylguanine-DNA methyltransferase activity, and failed to accumulate interstrand crosslinks in its DNA upon treatment with CNU. The subclone morphologically resembled its CNU-sensitive parental glioma cell strain. The close correlation between the increased cellular resistance, increased O-6-alkylguanine repair activity and the absence of crosslinking suggests that the formation of DNA crosslinks is one important mechanism of cytotoxicity produced by CNU, and that repair of DNA lesions by O-6-alkylguanine DNA alkyltransferase may partially prevent CNU-induced cytotoxicity.

Cell Line↗

PubMed2006

Pharmacological profiling of disulfiram using human tumor cell lines and human tumor cells from patients.

The thiocarbamate drug disulfiram has been used for decades in the treatment of alcohol abuse. Disulfiram induces apoptosis in a number of tumor cell lines and was recently by us proposed to act as a 26S proteasome inhibitor. In this work we characterized disulfiram in vitro with regard to tumor-type specificity, possible mechanisms of action and drug resistance and cell death in human tumor cell lines and in 78 samples of tumor cells from patients using the fluorometric microculture cytotoxicity assay and the automated fluorescence-imaging microscope ArrayScan((R)). Disulfiram induced cytotoxicity in a biphasic pattern in both cell lines and patient tumor cells. Disulfiram induced apoptosis as measured by cell membrane permeability, nuclear fragmentation/condensation and caspase-3/7 activation using high content screening assays. For many of the cell lines tested disulfiram was active in sub-micromolar concentrations. When comparing the logIC(50) patterns with other cytotoxic agents, disulfiram showed low correlation (R<0.5) with all drugs except lactacystin (R=0.69), a known proteasome inhibitor, indicating that the two substances may share mechanistic pathways. Disulfiram was more active in hematological than in solid tumor samples, but substantial activity was observed in carcinomas of the ovary and the breast and in non-small cell lung cancer. Disulfiram also displayed higher cytotoxic effect in cells from chronic lymphocytic leukemia than in normal lymphocytes (p<0.05), which may indicate some tumor selectivity. These results together with large clinical experience and relatively mild side effects encourage clinical studies of disulfiram as an anti-cancer agent.

Cell Line, Tumor↗

PubMed2000

[The expression and clinical significance of keratin 19, 20 mRNA in different tumor cell lines and tumor tissues].

OBJECTIVE: To study the expression of keratin 19, 20 (K19, K20) in different tumor cell lines and tumor tissues and its clinical implication. METHODS: Quantitative reverse transcription-polymerase chain reaction (RT-PCR) was employed to examine the specific expression of K19 and K20 mRNA in eleven tumor cell lines and 33 corresponding tumor tissue specimens. RESULTS: The expression of K19 mRNA was detected in 4 kinds of tumor cell lines and all tumor tissues examined, but the magnitude of expression differed, with a difference ranging from 1.7 to 10 folds for the same type of cancer. In some patients, the level of expression was as low as 12% of the positive control. K20 mRNA expression was negative for lung and esophageal tumor cell lines and the corresponding carcinoma specimens. In one of 6 bladder cancer specimens and in 4 of 5 colorectal cancer tissues, K20 expression was positive, at a level of 41%-77% of the positive control. There was no expression of K20 in bladder tumor cell line EJ1 and colorectal tumor cell line SW480. CONCLUSION: These results demonstrate that K19 and K20 may be used as a valuable marker for detecting circulating cancer cells, but the low level of expression in some cases of carcinoma would probably result in false negative results.

Biomarkers, Tumor↗

PubMed1992

Antiproliferative and antitumor activity of the 2-cyanoaziridine compound imexon on tumor cell lines and fresh tumor cells in vitro.

BACKGROUND: Imexon, a 2-cyanoaziridine, is therapeutic and reverses lymphadenopathy and splenomegaly in the LP-BM5 murine retrovirus-induced immunodeficiency disease (murine AIDS). It can restore chemotherapy-induced immunosuppression. Imexon reduced the incidence of lymphoma in severe combined immune deficient mice inoculated with human lymphocytes. PURPOSE: To determine its antitumor activity, we screened imexon against fresh human tumor cells and tumor cell lines. To determine the time-concentration relationships of its cytotoxicity, we studied the effects of imexon on macromolecular synthesis and on the cell cycle. METHODS: Imexon was incubated at 1-200 micrograms/mL with various tumor cell lines, mitogen-stimulated peripheral blood lymphocytes, and fresh tumor cells. Cell survival, macromolecular synthesis, and cell cycle progression were studied. RESULTS: The concentration of imexon that caused 50% inhibition of growth was under 10 micrograms/mL for lymphocytes stimulated with mitogens. It was about 3-10 micrograms/mL for B-cell lymphomas and both multi-drug-resistant and -sensitive myeloma cell lines. Imexon inhibited four of seven fresh lymphoma and 11 of 16 fresh myeloma biopsy specimens to less than 40% of the control. A 1-hour exposure of lymphoma cells to 50-100 microgram/mL followed by removal of drug by washing the cells and continuing culture resulted in greater than 95% inhibition during the next 48-72 hours. Imexon selectively inhibited protein synthesis during the first 24-48 hours of exposure of lymphoma and myeloma cells. Cells exposed to inhibitory concentrations of imexon were blocked in cell cycle progression. CONCLUSION: Imexon may be a potentially useful agent in the treatment of malignant disease, particularly lymphoid malignancies, and should be explored further.

Antineoplastic Agents↗

PubMed2004

A novel tumor cell line cloned from mutated human embryonic bone marrow mesenchymal stem cells.

A novel tumor cell line, denominated F6, was established from mutated human embryonic bone marrow mesenchymal stem cells (MSCs) which were induced by the GM-CSF and IL-4 in vitro. The characteristics of the F6 cell line, such as surface antigens, cell cycle, growth curve, gene expression, morphology, cytogenetics and tumor model were analyzed. The F6 cells were round and grew suspended in a plastic dish. The cell line has a strong self-renewal capability, was positive for CD13, CD29, CD44, but negative for CD1alpha, CD3, CD10, CD14, CD23, CD33, CD34, CD38, CD41, CD45, CD54 and HLA-DR. The surface antigens were lower than those of human embryonic MSCs. The karyotype of F6 cells was abnormal. The cell cycle included: G0/G1 phase, 52.24%; G2/M phase, 8.00%; S phase, 41.76%. After the cells had been passaged serially for more than 17 months (62 passages), their characteristics were still retained. The F6 cells resulted in tumors in SCID nude mice in vivo (8/8) and caused metastasis (3/8). The pathologic examination revealed that the tumor cells extensively invaded surrounding normal tissues such as dermis, muscular tissue, nerve tissue, adipose tissue and lymphoid tissue. F6 cell line, tumor tissues derived from F6 cells and the MSCs expressed different levels of the nucleostemin gene. These findings suggested that F6 may be a novel tumor cell line. It may provide evidence for the theory that cancer originates from stem cells, and may be useful for the investigation on safety of human MSCs in the clinical application.

Animals↗

PubMed2006

Pathway-specific differences between tumor cell lines and normal and tumor tissue cells.

BACKGROUND: Cell lines are used in experimental investigation of cancer but their capacity to represent tumor cells has yet to be quantified. The aim of the study was to identify significant alterations in pathway usage in cell lines in comparison with normal and tumor tissue. METHODS: This study utilized a pathway-specific enrichment analysis of publicly accessible microarray data and quantified the gene expression differences between cell lines, tumor, and normal tissue cells for six different tissue types. KEGG pathways that are significantly different between cell lines and tumors, cell lines and normal tissues and tumor and normal tissue were identified through enrichment tests on gene lists obtained using Significance Analysis of Microarrays (SAM). RESULTS: Cellular pathways that were significantly upregulated in cell lines compared to tumor cells and normal cells of the same tissue type included ATP synthesis, cell communication, cell cycle, oxidative phosphorylation, purine, pyrimidine and pyruvate metabolism, and proteasome. Results on metabolic pathways suggested an increase in the velocity nucleotide metabolism and RNA production. Pathways that were downregulated in cell lines compared to tumor and normal tissue included cell communication, cell adhesion molecules (CAMs), and ECM-receptor interaction. Only a fraction of the significantly altered genes in tumor-to-normal comparison had similar expressions in cancer cell lines and tumor cells. These genes were tissue-specific and were distributed sparsely among multiple pathways. CONCLUSION: Significantly altered genes in tumors compared to normal tissue were largely tissue specific. Among these genes downregulation was a major trend. In contrast, cell lines contained large sets of significantly upregulated genes that were common to multiple tissue types. Pathway upregulation in cell lines was most pronounced over metabolic pathways including cell nucleotide metabolism and oxidative phosphorylation. Signaling pathways involved in adhesion and communication of cultured cancer cells were downregulated. The three way pathways comparison presented in this study brings light into the differences in the use of cellular pathways by tumor cells and cancer cell lines.

Biosynthetic Pathways↗

PubMed2003

TRAIL/Apo2L ligands induce apoptosis in malignant rhabdoid tumor cell lines.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL/Apo2L) is a potent inducer of apoptosis in various cancer cells, whereas normal cells are not sensitive to TRAIL-mediated apoptosis. Four TRAIL/Apo2L receptors (DR4, DR5, DcR1, and DcR2) have been identified. DR4 and DR5 have a death domain, whereas DcR1 and DcR2 are called decoy receptors because of their incomplete or lack of a death domain. Malignant rhabdoid tumor (MRT) is an aggressive neoplasm showing a poor prognosis because of its resistance to chemotherapeutic agents. In this study, we examined whether TRAIL could induce apoptotic cell death in MRT cell lines. We found that although half of the MRT cell lines examined were sensitive to TRAIL/Apo2L, Western blot analysis revealed that the expression of DcR2 was low in TRAIL-sensitive MRT cells. We examined the effect of doxorubicin on the expression levels of TRAIL receptors and its enhancement on the susceptibility of MRT cell lines to TRAIL. Western blot and flow cytometric analyses revealed that doxorubicin significantly increased the expression of DR5, and somewhat up-regulated the expression of DR4 and DcR2. Moreover, doxorubicin, NF-kappaB inhibitor (SN50), and PI3-kinase/Akt inhibitor (wortmannin, LY294002) enhanced the susceptibility of MRT cell lines to TRAIL/Apo2L-induced apoptosis. These results suggest that TRAIL/Apo2L may provide the basis for clinical trials of TRAIL-based treatment to improve the outcome of MRT patients.

Animals↗