PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Cell Line, Tumor”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources
PubMed2002

Cystic fibrosis transmembrane conductance regulator modulates neurosecretory function in pulmonary neuroendocrine cell-related tumor cell line models.

The pulmonary neuroendocrine cell (PNEC) system consists of solitary cells and distinctive cell clusters termed neuroepithelial bodies (NEB) localized in the airway epithelium. PNEC/NEB express a variety of bioactive substances, including amine (serotonin, 5HT) and neuropeptides. We have previously shown that NEB cells are O(2) sensors expressing nicotinamide adenine diphosphate oxidase complex and O(2) sensitive K(+) channel. Recently, we demonstrated expression of functional cystic fibrosis transmembrane conductance regulator (CFTR) and Cl(-) conductances in NEB cells of rabbit neonatal lung. Because PNEC/NEB are sparsely distributed and difficult to study in native lung, we investigated small-cell lung carcinoma (SCLC) and carcinoid tumor cell lines (tumor counterparts of normal PNEC/NEB) as models for PNEC/NEB. SCLC (H146, H345) and carcinoid (H727) cell lines express neuroendocrine cell markers, including chromogranin A, neural cell adhesion molecule (N-CAM), 5HT, and tryptophan hydroxylase. We report that H146, H345, and H727 express CFTR messenger RNA (reverse transcription polymerase chain reaction) and protein (immunoblotting) and possess functional CFTR Cl(-) conductance, demonstrated by an iodide efflux assay inhibitable by transfection with antisense CFTR. Using an immunoassay to quantitate 5HT secretion, we also show that downregulation of CFTR abolishes hypoxia-induced 5HT release, and reduces secretory response to high potassium. Our findings suggest that CFTR may modulate neurosecretory activity of PNEC/NEB possessing O(2) sensor function. We propose that these tumor cell lines may be useful models for investigating the role of CFTR in PNEC/NEB functions in health and disease.

Biomarkers↗
PubMed1976

Surface marker characteristics and Epstein-Barr virus studies of two established North American Burkitt's lymphoma cell lines.

Tumor cell lines have been established in continuous culture from two North American Burkitt's lymphomas. The SU-AmB-1 line, derived from a patient with low serum antibody titers to Epstein-Barr virus (EBV), was devoid of EBV genomes by the reaction for EBV-associated nuclear antigen (EBNA), could not be induced to express EBV antigens, and was highly refractory to EBV superinfection. Conversely, the SU-AmB-2 cell line, derived from a patient with "African type" serology, yielded a positive EBNA reaction and was readily inducible and superinfectable. Although both cell lines possessed B (bone-marrow-derived) cell characteristics, they had different surface marker patterns. It is postulated that two different classes of undifferentiated B cell lymphomas exist, one of which is positive for the presence of EBV genomes and occurs endemically in Africa and New Guinea and sporadically in other parts of the world, the other of which is EBV-negative and occurs sporadically throughout the world, including the endemic areas.

Adolescent↗
PubMed2005

Growth sensitivity of a recombinant simian virus 5 P/V mutant to type I interferon differs between tumor cell lines and normal primary cells.

A paramyxovirus SV5 mutant (rSV5-P/V-CPI-) that encodes 6 naturally-occurring P/V gene substitutions is a potent inducer of type I interferon (IFN) and is restricted for low moi growth, two phenotypes not seen with WT SV5. In this study, we have compared the IFN sensitivity of WT SV5 and the rSV5-P/V-CPI- mutant in tumor cell lines and in cultures of normal primary cells. We have tested the hypothesis that differences in IFN induction elicited by WT rSV5 and rSV5-P/V-CPI- are responsible for differences in low moi growth and spread. In contrast to WT SV5, low moi infection of A549 lung carcinoma cells with rSV5-P/V-CPI- resulted in a plateau of virus production by 24-48 h pi when secreted IFN levels were between approximately 100 and 1000 U/ml. Gene microarray and RT-PCR analyses identified IFN genes and IFN-stimulated genes whose expression were increased by infection of A549 cells with WT and P/V mutant viruses. Restricted low moi growth and spread of rSV5-P/V-CPI- in A549 cells was relieved in the presence of neutralizing antibodies to IFN-beta but not TNF-alpha. When A549 or MDA-MB-435 breast tumor cells were pretreated with IFN, both WT and P/V mutant viruses showed delayed spread and approximately 10-fold reduction in virus yield, but infections were not eliminated. Using normal primary human epithelial cells that have undergone limited passage in culture, WT rSV5 and rSV5-P/V-CPI- displayed high moi growth properties that were similar to that seen in A549 cells. However, IFN pretreatment of these primary cells as well as normal human lung cells eliminated low moi spread of both mutant and WT rSV5 infections. Together, these data demonstrate that SV5 growth in normal primary human cells is highly sensitive to IFN compared to growth in some tumor cell lines, regardless of whether the P/V gene is WT or mutant. These results suggest a model in which spread of WT SV5 in normal human cells is dependent on the ability of the virus to prevent IFN synthesis. The implications of these results for the use of recombinant paramyxoviruses as vectors are discussed.

Cell Line, Tumor↗
PubMed1995

Suppression of the tumorigenic phenotype of a rat liver epithelial tumor cell line by the p11.2-p12 region of human chromosome 11.

Comparative chromosomal mapping studies and investigations of tumor-associated chromosomal abnormalities suggest that the development of hepatic tumors in humans and rats may share a common molecular mechanism that involves inactivation of the same tumor suppressor genes or common genetic loci. We investigated the potential of human chromosomes 2 and 11 to suppress the tumorigenic phenotype of rat liver epithelial tumor cell lines. These tumor cell lines (GN6TF and GP7TB) display elevated saturation densities in culture, efficiently form colonies in soft agar, and produce subcutaneous tumors in 100% of syngeneic rat hosts with short latency periods. Introduction of human chromosome 11 by microcell fusion markedly altered the tumorigenicity and the transformed phenotype of GN6TF cells. In contrast, the tumorigenic potential and phenotype of GP7TB cells was unaffected by the introduction of human chromosome 11, indicating that not all rat liver tumor cell lines can be suppressed by loci carried on this chromosome. Introduction of human chromosome 2 had little or no effect on the tumorigenicity or cellular phenotype of either tumor cell line, suggesting the involvement of chromosome 11-specific loci in the suppression of the GN6TF tumor cell line. The GN6TF-11neo microcell hybrid cell lines displayed significantly reduced saturation densities in monolayer cultures, and their ability to grow in soft agar was completely inhibited. Although GN6TF-11neo cells ultimately formed tumors in 80-100% of syngeneic rat hosts, the latency period for tumor formation was much longer. Molecular characterization of GN6TF-11neo microcell hybrid cell lines indicated that some of the clonal lines had spontaneously lost significant portions of the introduced human chromosome, partially delineating the chromosomal location of the putative tumor suppressor locus to the region between the centromere and 11p12. Molecular examination of microcell hybrid-derived tumor cell lines further defined the minimal portion of human chromosome 11 capable of tumor suppression in this model system to the region 11p11.2-p12.

Animals↗
PubMed1994

[Expression of integrin molecule in urological tumor cell lines by using RT-PCR method].

Integrins are heterodimer molecule that are composed of one alpha subunit and one beta subunit. Integrins appear to be the major receptors by which cells attach to extracellular matrices, and some integrins also mediate important cell-cell adhesion event. In recent years signaling pathway via beta subunit of integrin molecule has been clarified, and 8 kinds of integrin beta subunit are known to exist. And so we investigated the expression of integrin beta subunit in various urological tumor cell lines by using RT-PCR method. Materials are composed of 8 renal cell carcinoma cell lines, 2 urinary bladder carcinoma cell lines, a testicular tumor cell line and a prostate tumor cell line. All 12 cell lines express integrin beta 1 subunit. The expression rate of beta 4 subunit in renal cell carcinoma lines are lower than that in other urological tumor cell lines. The expression of beta 6 subunit was observed in renal cell carcinoma cell lines and testicular tumor line. In testicular tumor cell line we also found the expression of beta 2 subunit which expression had been believed to be specific in leukocyte.

Base Sequence↗
PubMed2004

MIP-3alpha transfection into a rodent tumor cell line increases intratumoral dendritic cell infiltration but enhances (facilitates) tumor growth and decreases immunogenicity.

Dendritic cells are powerful APCs for activation of specific antitumor T lymphocytes. To present tumor Ags efficiently, they have first to migrate to the tumor site, engulf Ag, and then process them. To attract immature DCs to the tumor site, we transfected tumor cells with MIP-3alpha which is strongly chemotactic for DCs. Surprisingly, MIP-3alpha-transfected tumor cells grew faster than the mock-transfected tumor cells. Histological analysis and tumor dissociation confirmed that the MIP-3alpha-transfected tumors contain three to four times more DCs than mock-transfected tumors. FACS analysis of the intratumor DCs showed that they were predominantly immature. Functional analysis showed that the alloreactivity mediated by these infiltrating MIP-3alpha-transfected tumor DCs is strongly reduced. In conclusion, MIP-3alpha is an efficient chemokine for attracting DCs in vivo, but the high density of DCs in the tumor site injection is not a sufficient condition to induce an immune response. Furthermore, this attraction of immature DCs may always have an adverse effect by inducing a tolerance to the tumor cells.

Animals↗
PubMed1987

Secretion of antileucoprotease from a human lung tumor cell line.

Two human tumor cell lines were analyzed for the production of human antileucoprotease (ALP). One of them, a human squamous lung carcinoma cell line (HS-24) synthesized, as confirmed by Western blot analysis, high amounts of ALP in serum-free medium. The supernatant inhibited elastase, chymotrypsin and trypsin. Northern blot analysis with an 18-mer radiolabelled oligonucleotide, derived from an ALP specific cDNA clone, revealed a specific mRNA of about 700-800 nucleotides in HS-24 tumor cells. In contrast, a secondary human lung tumor cell line (SB-3), derived from the adrenal cortex, did not synthesize ALP when assayed under identical conditions. The supernatant inhibited only trypsin and chymotrypsin.

Carcinoma, Squamous Cell↗
PubMed1995

VEGF mRNA is reversibly stabilized by hypoxia and persistently stabilized in VEGF-overexpressing human tumor cell lines.

Solid tumor growth is dependent upon angiogenesis, a process by which soluble factors released from a tumor induce the sprouting and growth of new blood vessels from nearby venules into the tumor. This process of tumor vascularization provides tumor cells with nutrients, oxygen, and an enhanced ability to establish metastasis at peripheral sites by migration through the circulatory system. Vascular endothelial growth factor is a potent angiogenic factor that is expressed at low levels by most normal cells, can be upregulated in normal cells by exposure to hypoxia or phorbol esters, and exhibits high levels of constitutive expression in some human tumors and tumor cell lines. The mechanism underlying the stable change that results in VEGF overexpression in tumors is unknown. Here, we demonstrate that both hypoxia and TPA induce stabilization of VEGF mRNA, that stabilization by hypoxia is rapidly reversible upon reexposure to normoxia, and that tumor cell lines exhibiting constitutive overexpression of VEGF also exhibit constitutive stabilization of VEGF transcripts. Stabilized VEGF transcripts in tumor cells are refractile or nearly refractile toward further stabilization by TPA or hypoxia, respectively. Furthermore, cycloheximide induces stabilization of VEGF mRNA in normal cells but has no effect on VEGF transcript stability in tumor cells that contain stabilized transcripts. These results suggest that normal signal transduction mechanisms mediate stabilization of the VEGF mRNA, and that mutations in this regulatory pathway in tumor cells may lead to chronic message stabilization, overexpression of VEGF proteins, and ensuing tumor vascularization.

Animals↗
PubMed2004

TNF-alpha-mediated apoptosis in normal human prostate epithelial cells and tumor cell lines.

In this study we compared the role of TNF-alpha in the regulation of growth and apoptosis in normal human prostate epithelial cells (NP) and prostate tumor cell lines PC3 and LNCap. The NP and PC3 cells were resistant whereas the LNCap cell line was highly sensitive to TNF-alpha induced growth arrest and apoptosis. The resistance of NP and PC3 cells was mediated via an NF-kB survival pathway as treatment of resistant cells with TNF-alpha was accompanied by phosphorylation of I-kBalpha and translocation of NF-kB to the nucleus. TNF-alpha did not induce phosphorylation of I-kB in the sensitive LNCap cells. The sensitivity of LNCap cells involved a cysteine protease cascade as Z-VAD-CH2 F reversed the sensitivity of LNCap cells and induced resistance to TNF-alpha. The differences in susceptibilities to TNF-alpha induced apoptosis of NP and certain prostate tumor cells offer intriguing possibilities for the treatment of prostate cancer without affecting the normal prostate tissue.

Active Transport, Cell Nucleus↗
PubMed2005

Primary human lymphocytes transduced with NY-ESO-1 antigen-specific TCR genes recognize and kill diverse human tumor cell lines.

cDNAs encoding TCR alpha- and beta-chains specific for HLA-A2-restricted cancer-testis Ag NY-ESO-1 were cloned using a 5'RACE method from RNA isolated from a CTL generated by in vitro stimulation of PBMC with modified NY-ESO-1-specific peptide (p157-165, 9V). Functionality of the cloned TCR was confirmed by RNA electroporation of primary PBL. cDNA for these alpha- and beta-chains were used to construct a murine stem cell virus-based retroviral vector, and high titer packaging cell lines were generated. Gene transfer efficiency in primary T lymphocytes of up to 60% was obtained without selection using a method of precoating retroviral vectors onto culture plates. Both CD4(+) and CD8(+) T cells could be transduced at the same efficiency. High avidity Ag recognition was demonstrated by coculture of transduced lymphocytes with target cells pulsed with low levels of peptide (<20 pM). TCR-transduced CD4 T cells, when cocultured with NY-ESO-1 peptide pulsed T2 cells, could produce IFN-gamma, GM-CSF, IL-4, and IL-10, suggesting CD8-independent, HLA-A2-restricted TCR activation. The transduced lymphocytes could efficiently recognize and kill HLA-A2- and NY-ESO-1-positive melanoma cell lines in a 4-h (51)Cr release assay. Finally, transduced T cells could efficiently recognize NY-ESO-1-positive nonmelanoma tumor cell lines. These results strongly support the idea that redirection of normal T cell specificity by TCR gene transfer can have potential applications in tumor adoptive immunotherapy.

Adoptive Transfer↗
PubMed1993

Characterization of human tumor cell lines transduced with the cDNA encoding either tumor necrosis factor alpha (TNF-a) or interleukin-2 (IL-2).

Tumor cell lines were generated from cancer patients, 17 with metastatic melanoma and one with colon adenocarcinoma. The lines were characterized as tumor cells by the presence of tumor associated antigens demonstrated by indirect immunofluorescence and analysing using a fluorescence activated cell sorter (FACS). The tumor cell lines were transduced using retroviruses encoding neomycin phosphotransferase and either human tumor necrosis factor alpha (TNF-alpha) or interleukin-2 (IL-2). Following transduction, cells were selected and grown in the neomycin analogue G418. Fibroblasts overgrew tumor cells in 6/18 cases following selection in G418 and 1/18 lines did not grow at all after selection. In the remaining 11 lines the expression of tumor associated antigens, growth, and susceptibility to lysis by LAK cells was similar between the selected transduced tumor cell lines and the nontransduced controls. Of the lines tested, all were positive for the presence of the cytokine gene by Southern blot or PCR analysis. In addition, no replication competent retrovirus was detected in the cell lines following transduction using an extended mink S+L- focus assay. The amount of specific cytokine produced per 10(5) transduced tumor cells in 24 h ranged from 0.2 ng to 5.8 ng of TNF-alpha for the TNF transduced lines and from 0.1 ng to 3.6 ng of IL-2 for the IL-2 transduced tumor cell lines. One transduced tumor cell line examined maintained consistent levels of cytokine production when studied at 15 different time intervals over a period of 198 days. Additionally, 40,000 rads of gamma irradiation did not stop cytokine production from two transduced tumor cell lines when studied over 6 days. This study demonstrates the feasibility of growing human tumor cell lines from surgical biopsies and genetically modifying those lines to produce a cytokine of choice for possible use as a tumor cell vaccine.

Adenocarcinoma↗
PubMed1990

In vitro synergistic activity of 5-fluorouracil with low-dose ozone against a chemoresistant tumor cell line and fresh human tumor cells.

We followed the concept that the chemical reactivity of ozone depends upon its oxidative properties. Activated oxygen species are causally involved in toxicity of certain chemotherapeutic drugs. We have tested this prediction in human cell cultures either to overcome chemoresistance and/or to increase chemical cytotoxicity. Our results indicate that ozone in combination with 5-fluorouracil (5-FU) makes a 5-FU-resistant cell line susceptible for the combined treatment modality. Furthermore, ozone acts synergistically or at least additive to chemotherapy in different tumor cell suspensions, derived from the breast and the colon.

Dose-Response Relationship, Drug↗
PubMed1990

[Ultrastructure of cultured normal bladder transitional epithelial cell and BBN induced rat bladder tumor cell lines].

A normal rat bladder transitional epithelial cell line and seven tumor cell lines cultured from tumor induced by 0.05% N-Butyl-N-4-hydroxybutyl-Nitrosamine (BBN) were established and a comparative study on the doubling time and Ultrastructure of the cultured cell lines was performed. 1. Seven cultured cell lines (TU-B1 1-7) were obtained from bladder tumors induced by the administration of BBN for 32 weeks. 2. The doubling time of the cultured tumor cell lines were 43, 24, 28, 24, 25, 31, and 45 hours, suspectively. 3. These cultured tumor cell line were inoculated subcutaneously into nude mice and transitional epithelial carcinomas differing in degree of differentiation were observed. 4. Horizontal and tangential sections of these cultured tumor cell lines were examined by transmission electron microscopy. The development of intracellular organella and the presence of microvilli on the surface of the cells were noted. Intracellular adhesion was poor but the morphological characteristics of bladder transitional epithelium with compressed vesicles and other intracellular structures such as desmosome and free ribosomes were observed. 5. By applying the attached collagen gel method to our cell lines, it was possible to obtain cultured rat epithelial cells with the same morphology as in vivo, in addition to the tumor cell lines. 6. These cultured cell lines of normal rat transitional epithelium appear to be useful a experimental models with which one could clarify the function of the transitional epithelium and the mechanisms of bladder carcinogenesis.

Animals↗
PubMed2005

Nuclear location-dependent role of peripheral benzodiazepine receptor (PBR) in hepatic tumoral cell lines proliferation.

PBR is involved in numerous biological functions, including steroid biosynthesis, mitochondrial oxidative phosphorylation and cell proliferation. The presence of PBR at the perinuclear/nuclear subcellular level has been demonstrated in aggressive breast cancer cell lines and human glioma cells where it seems to be involved in cell proliferation. In our study we investigated the presence of perinuclear/nuclear PBR in different hepatic tumor cell lines with regard to binding to [3H] PK 11195 and protein analysis. The results obtained by saturation binding experiments and scatchard analysis of perinuclear/nuclear PBR density in parallel with the results on the growth curves of the cell lines tested, indicate that the perinuclear/nuclear PBR density correlates inversely with cell doubling time. Moreover, the cell line with high perinuclear/nuclear PBR proliferated in response to PBR ligand, whereas that with low perinuclear/nuclear PBR did not. Our results reinforce the idea that the subcellular localisation of PBR defines its function and that this receptor could be a possible target for new strategies against cancer.

Active Transport, Cell Nucleus↗
PubMed1997

Conditional mutator phenotypes in hMSH2-deficient tumor cell lines.

Two human tumor cell lines that are deficient in the mismatch repair protein hMSH2 show little or no increase in mutation rate relative to that of a mismatch repair-proficient cell line when the cells are maintained in culture conditions allowing rapid growth. However, mutations accumulate at a high rate in these cells when they are maintained at high density. Thus the mutator phenotype of some mismatch repair-deficient cell lines is conditional and strongly depends on growth conditions. These observations have implications for tumor development because they suggest that mutations may accumulate in tumor cells when growth is limited.

Cell Count↗
PubMed2005

Overexpression of cyclin D1 promotes tumor cell growth and confers resistance to cisplatin-mediated apoptosis in an elastase-myc transgene-expressing pancreatic tumor cell line.

PURPOSE: Elevated cyclin D1 in human pancreatic cancer correlates with poor prognosis. Because pancreatic cancer is invariably resistant to chemotherapy, the goal of this study was to examine whether the drug resistance of pancreatic cancer cells is in part attributed to cyclin D1 overexpression. EXPERIMENTAL DESIGN: Stable overexpression and small interfering RNA (siRNA)--mediated knockdown of cyclin D1 were done in the newly established Ela-myc pancreatic tumor cell line. Cisplatin sensitivity of control, overexpressing, and siRNA-transfected cells was determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, clonogenic, and apoptotic assays [DNA fragmentation, sub-G1, and poly(ADP-ribose) polymerase cleavage analysis]. The role of nuclear factor-kappaB and apoptotic proteins in cyclin D1-mediated chemoresistance was examined by EMSA and Western blotting, respectively. RESULTS: Overexpression of cyclin D1 in Ela-myc pancreatic tumor cells promoted cell proliferation and anchorage-independent growth. Moreover, cyclin D1-overexpressing cells exhibited significantly reduced chemosensitivity and a higher survival rate upon cisplatin treatment, as determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and clonogenic assays, respectively. Although overexpression of cyclin D1 rendered cells more resistant to cisplatin-induced apoptosis, siRNA-directed suppression of cyclin D1 expression resulted in enhanced susceptibility to cisplatin-mediated apoptosis. The attenuation of cisplatin-induced cell death in cyclin D1-overexpressing cells was correlated with the up-regulation of nuclear factor-kappaB activity and maintenance of bcl-2 and bcl-xl protein levels. CONCLUSIONS: These results suggest that overexpression of cyclin D1 can contribute to chemoresistance of pancreatic cancer cells because of the dual roles of cyclin D1 in promoting cell proliferation and in inhibiting drug-induced apoptosis.

Animals↗