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Cell Carcinoma Cell Lines (cell + carcinoma_cell_line)
Kinds of Cell Carcinoma Cell Lines Selected AbstractsApoptosis induction by interleukin-2-activated cytotoxic lymphocytes in a squamous cell carcinoma cell line and Daudi cells , involvement of reactive oxygen species-dependent cytochrome c and reactive oxygen species-independent apoptosis-inducing factorsIMMUNOLOGY, Issue 2 2003Tetsuya Yamamoto Summary Investigation of the induction of apoptosis by cytotoxic lymphocytes has mainly focused on the signalling associated with Fas and its adaptor proteins. The signal pathway via mitochondria, however, has not been sufficiently elucidated in cytotoxic lymphocyte-induced apoptosis. We examined the release of mitochondrial proapoptotic factors by lymphokine-activated killer (LAK) cells in two cell lines. LAK cell-induced DNA fragmentation of the target cells was suppressed to approximately 50% of control levels by the addition of neutralizing monoclonal antibody to Fas and a granzyme B inhibitor. When intracellular reactive oxygen species (ROS) were scavenged, the LAK cell-induced DNA fragmentation was decreased to approximately 60% of the non-treated cell level. Co-cultivation of Daudi cells with LAK cells increased cytosolic and mitochondrial ROS levels. Activation of procaspase-3 and apoptosis by treatment of oral squamous cell carcinoma cells (OSC) with LAK cells was partially inhibited by pretreatment of OSC cells with ROS scavengers and mitochondrial complex inhibitors. Furthermore, cytochrome c and apoptosis-inducing factor (AIF) were released from mitochondria by OSC cell treatment with supernatants of LAK cells. The supernatant-induced cytochrome c release was suppressed by mitochondrial complex inhibitors, but the inhibitors did not inhibit the release of AIF. These results indicate that LAK cells induce target cell apoptosis via not only the Fas/Fas ligand system and granzyme B, but also ROS-dependent cytochrome c and ROS-independent AIF release. [source] p120 catenin is associated with desmogleins when desmosomes are assembled in high-Ca2+ medium but not when disassembled in low-Ca2+ medium in DJM-1 cellsTHE JOURNAL OF DERMATOLOGY, Issue 6 2008Miho KANNO ABSTRACT We recently showed that p120 catenin (p120ctn), which is an armadillo family protein member that binds to E-cadherin (E-cad), is also localized to desmosomes by directly or indirectly binding to desmogleins (Dsg). We examined whether p120ctn is associated with Dsg1 and Dsg3, as compared with E-cad and plakoglobin (PG), in keratinocytes grown in high or low Ca2+, using a human squamous cell carcinoma cell line, DJM-1 cells. The cell lysate of DJM-1 cells grown in high- or low-Ca2+ media was immunoprecipitated with anti-Dsg1/2 and Dsg3 antibodies, and we examined whether p120ctn is associated with Dsg1 and Dsg3. Then, we observed the co-localization between Dsg3 and p120ctn in cells grown in high- or low-Ca2+ medium on double-staining immunofluorescence microscopy using anti-p120ctn and anti-Dsg3 antibodies. Immunoprecipitates with anti-Dsg1/2 and Dsg3 antibodies in cells grown in high-Ca2+ medium contained p120ctn. In contrast, in low-Ca2+ medium, p120ctn was co-immunoprecipitated with neither Dsg1 nor Dsg3, but was co-immunoprecipitated with E-cad in cells grown in both high- and low-Ca2+ media. Dsg3 was associated with PG in cells grown in both low- and high-Ca2+ media. On immunofluorescence microscopy, p120ctn and Dsg3 were independently observed in cells grown in low-Ca2+ medium; p120ctn, but not Dsg3, was observed in a linear pattern at the cell,cell boundary. However, they were co-localized at cell,cell contacts in cells grown in high-Ca2+ medium. Thus, these proteins are not co-localized in low Ca2+ medium. These results suggest that p120ctn plays an important role in Ca2+ -induced desmosome formation. [source] Role of Nitric Oxide in the Development of Distant Metastasis From Squamous Cell Carcinoma,THE LARYNGOSCOPE, Issue 2 2007Richard L. Scher MD Abstract Background: Metastasis, the dissemination of malignant cells to distant sites, remains one of the most significant factors responsible for death from cancer. Recent studies have shown some improvement in the rate of distant metastasis (DM) with the addition of chemotherapy to surgery and radiation for treatment of head and neck squamous cell carcinoma (HNSCC). However, diagnosis and treatment at an early stage ultimately leads to a better prognosis. The prediction of which patients will develop metastasis and the selection of treatment most effective at preventing and treating metastasis remains dependent on an incomplete understanding of prognostic factors and the biological and molecular basis for metastatic development. This study was undertaken using an in vivo model to investigate the possible role of nitric oxide (NO) in the development of metastasis from HNSCC. The findings will result in better understanding of the metastatic process for HNSCC, with the potential to develop and implement therapies that could prevent and treat metastasis in patients. Objectives/Hypothesis: 1) To analyze whether in vivo videomicroscopy (IVVM) is useful for the study of DM from squamous cell carcinoma of the head and neck; 2) with use of IVVM, investigate the effect of the biological mediators NO and interleukin (IL)-1 on the adhesion of circulating human HNSCC cells in the hepatic microcirculation. Study Design: Prospective study using an animal model. Methods: Phase 1: athymic nude rats and mice were used for IVVM experiments. The cremaster muscle and liver, used as arterial and venous flow models, were tested to determine whether IVVM was useful for the study of human HNSCC interactions with the microcirculation. A human squamous cell carcinoma cell line (FaDu) labeled with the intracytoplasmic fluorescent marker BCECF-am. was used for all experiments. Videomicroscopic images of FaDu cells in the microcirculation were analyzed for cell adhesion, morphology, deformation, circulation, location of adhesion within the microcirculation, and alteration of microvascular circulation. Phase 2: the effect of IL-1, NO, and NO inhibitors on HNSCC cell adhesion in the hepatic microcirculation of nude mice was analyzed by IVVM. This was followed by histologic determination of the ratio of FaDu cells present for liver area analyzed. Nude mice were treated with 1) IL-1; 2) L-arginine (an NO substrate); or 3) L-N-monomethyl-L-arginine (an NO synthase inhibitor) alone or in combination. These data were analyzed statistically to determine the effect on cell adhesion in the liver. Results: IVVM provided a method for the study of circulating HNSCC with the microcirculation in both the cremaster and liver models. FaDu cells were arrested at the inflow side of the circulation, with maintenance of cell integrity. L-arginine and IL-1 both increased FaDu cell arrest in the liver above baseline (P = .00008 and P = .03), and the combination of these agents potentiated the effect (P = .000009). Conclusions: IVVM allows direct assessment of circulating HNSCC with the microcirculation and is a powerful model for the study of DM. NO and IL-1 play a role in increasing the arrest of HNSCC in the liver and are important in the generation of DM in patients with HNSCC. [source] Carbon-ion beam treatment induces systemic antitumor immunity against murine squamous cell carcinomaCANCER, Issue 15 2010Akinao Matsunaga MD Abstract BACKGROUND: Carbon-ion beam (CIB) treatment is a powerful tool for controlling primary tumors in the clinical setting. However, to date, few clinical or experimental studies have investigated the effects of CIB treatment on tumor recurrence and antitumor immunity. METHODS: A multiple challenge test was performed using syngenic and nude mouse models of a poorly immunogenic squamous cell carcinoma cell line (SCCVII) after CIB treatment at a clinically available dose (77 kiloelectron volts [keV]/,m) to primary tumors. To further examine changes in antitumor immunity in this model, the authors used dendritic cell (DC)-based immunotherapy. RESULTS: In a syngenic model, CIB treatment itself resulted not only in efficient elimination of the primary tumor but also in a dramatic reduction of tumor formation after secondary tumor challenge at a contralateral site (P < .0001). Conversely, CIB treatment eliminated neither the primary nor the secondary tumor in nude mice. This antitumor effect produced by CIB treatment was enhanced significantly by combining it with DC immunotherapy (P = .0007). Combined CIB and DC treatment induced more intense cytolytic activity than CIB in a chromium-release assay. The third challenge tests, which included challenge with a third-party tumor cell line (FM3A) and effector depletion, revealed that the antitumor effects were the results of tumor-specific, long-lasting antitumor immunity through CD8-positive T lymphocytes. CONCLUSIONS: To the authors' knowledge, this is the first demonstration of strong antitumor immunity induced by CIB treatment in a dermal tumor, and this effect was enhanced by combining it with DC-based immunotherapy. The authors concluded that this combination warrants further investigation as a promising modality for the prevention of tumor recurrence. Cancer 2010. © 2010 American Cancer Society. [source] Epidermal growth factor-dependent enhancement of invasiveness of squamous cell carcinoma of the breastCANCER SCIENCE, Issue 5 2010Fuyo Kimura Factors that promote the aggressiveness of squamous cell carcinoma of the breast are not well understood. To examine the involvement of cell motility and the mechanism of this behavior, a squamous cell carcinoma cell line of the breast (HBC9) was established from a metastatic lymph node of a Japanese woman. HBC9 expressed epidermal growth factor receptor (EGFR), but was negative for Her2 or Her3. The invasive ability of HBC9 was compared with that of four breast ductal carcinoma cell lines by Matrigel invasion assay. EGF stimulation induced the formation of surface protrusions and cell migration in HBC9 cells, and significantly increased the number of cells migrating through the Matrigel. The invasive ability of HBC9 was compared with other cell lines of breast carcinoma; it was much greater than that of MCF-7, BT474, or HBC5, but did not differ significantly from that of MDA-MB-231. Observation of the surface protrusions of HBC9 by confocal laser microscopy revealed co-localization of Arp2 and N-WASP with actin polymerization, detected by visualization with phalloidin, indicating that the protrusions induced by EGF were invadopodia. In HBC9 cells, cortactin also co-localized with the N-WASP/Arp2/3 complex in the protrusions. Immunohistochemistry of 12 cases of squamous cell carcinoma of the breast revealed expression of cortactin and EGFR in all of them, and this was confirmed by western blotting in two cases. These results suggest that EGF-dependent enhancement of cell motility by formation of invadopodia associated with cortactin is a cause of the clinical aggressiveness of squamous cell carcinoma of the breast. (Cancer Sci 2010; 101: 1133,1140) [source] Identification of candidate genes involved in the radiosensitivity of esophageal cancer cells by microarray analysisDISEASES OF THE ESOPHAGUS, Issue 4 2008R. Ogawa SUMMARY., Radiotherapy plays a key role in the control of tumor growth in esophageal cancer patients. To identify the patients who will benefit most from radiation therapy, it is important to know the genes that are involved in the radiosensitivity of esophageal cancer cells. Hence, we examined the global gene expression in radiosensitive and radioresistant esophageal squamous cell carcinoma cell lines. Radiosensitivities of 13 esophageal cancer cell lines were measured. RNA was extracted from each esophageal cancer cell line and a normal esophageal epithelial cell line, and the global gene expression profiles were analyzed using a 34 594-spot oligonucleotide microarray. In the clonogenic assay, one cell line (TE-11) was identified to be highly sensitive to radiation, while the other cell lines were found to be relatively radioresistant. We identified 71 candidate genes that were differentially expressed in TE-11 by microarray analysis. The up-regulated genes included CABPR, FABP5, DSC2, GPX2, NME, CBR3, DOCK8, and ABCC5, while the down-regulated genes included RPA1, LDOC1, NDN, and SKP1A. Our investigation provided comprehensive information on genes related to radiosensitivity of esophageal cancer cells; this information can serve as a basis for further functional studies. [source] Hyperphosphorylation of replication protein A in cisplatin-resistant and -sensitive head and neck squamous cell carcinoma cell linesHEAD & NECK: JOURNAL FOR THE SCIENCES & SPECIALTIES OF THE HEAD AND NECK, Issue 5 2010Karoline C. Manthey MS Abstract Background Resistance to chemotherapy is a major limitation in the treatment of head and neck squamous cell carcinomas (HNSCCs), accounting for high mortality rates in patients. Here, we investigated the role of replication protein A (RPA) in cisplatin and etoposide resistance. Methods We used 6 parental HNSCC cell lines. We also generated 1 cisplatin-resistant progeny subline from a parental cisplatin-sensitive cell line, to examine cisplatin resistance and sensitivity with respect to RPA2 hyperphosphorylation and cell-cycle response. Results Cisplatin-resistant HNSCC cell levels of hyperphosphorylated RPA2 in response to cisplatin were 80% to 90% greater compared with cisplatin-sensitive cell lines. RPA2 hyperphosphorylation could be induced in the cisplatin-resistant HNSCC subline. The absence of RPA2 hyperphosphorylation correlated with a defect in cell-cycle progression and cell survival. Conclusion Loss of RPA2 hyperphosphorylation occurs in HNSCC cells and may be a marker of cellular sensitivities to cisplatin and etoposide in HNSCC. © 2009 Wiley Periodicals, Inc. Head Neck, 2010 [source] Head and neck squamous cell carcinoma cell lines: Established models and rationale for selectionHEAD & NECK: JOURNAL FOR THE SCIENCES & SPECIALTIES OF THE HEAD AND NECK, Issue 2 2007Charles J. Lin BA Abstract Background. Head and neck squamous cell carcinoma (HNSCC) cell lines are important preclinical models in the search for novel and targeted therapies to treat head and neck cancer. Unlike many other cancer types, a wide variety of primary and metastatic HNSCC cell lines are available. An easily accessible guide that organizes important characteristics of HNSCC cell lines would be valuable for the selection of appropriate HNSCC cell lines for in vitro or in vivo studies. Methods. A literature search was performed. Results. Cell growth and culture parameters from HNSCC cell lines were catalogued into tables or lists of selected characteristics. Methods for establishing cancer cell lines and basic cell culture maintenance techniques were reviewed. Conclusions. A compendium of HNSCC cell line characteristics is useful for organizing the accumulating information regarding cell line characteristics to assist investigators with the development of appropriate preclinical models. © 2006 Wiley Periodicals, Inc. Head Neck, 2006 [source] DNA methylation and histone modifications cause silencing of Wnt antagonist gene in human renal cell carcinoma cell linesINTERNATIONAL JOURNAL OF CANCER, Issue 3 2008Ken Kawamoto Abstract Secreted frizzled-related protein 2 (sFRP2) is a negative modulator of the Wingless-type (Wnt) signaling pathway, and shown to be inactivated in renal cell carcinoma (RCC). However, the molecular mechanism of silencing of sFRP2 is not fully understood. Our study was designed to elucidate the silencing mechanism of sFRP2 in RCC. Expression of sFRP2 was examined in 20 pairs of primary cancers by immunohistochemistry. Kidney cell lines (HK-2, Caki-1, Caki-2, A-498 and ACHN) were analyzed for sFRP2 expression using real-time RT-PCR and Western blotting. The methylation status at 46 CpG sites of the 2 CpG islands in the sFRP2 promoter was characterized by bisulfite DNA sequencing. Histone modifications were assessed by chromatin immunoprecipitation (ChIP) assay using antibodies against AcH3, AcH4, H3K4 and H3K9. sFRP2 was frequently repressed in primary cancers and in RCC cells. The majority of sFRP2 negative cells had a methylated promoter. Meanwhile, sFRP2 expression was repressed by a hypomethylated promoter in Caki-1 cells, and these cells had a repressive histone modification at the promoter. In Caki-1 cells, sFRP2 was reactivated by trichostatin A (TSA). Repressive histone modifications were also observed in RCC cells with hypermethylated promoters, but sFRP2 was reactivated only by 5-aza-2,-deoxycytidine (DAC) and not by TSA. However, the activation of the silenced sFRP2 gene could be achieved in all cells using a combination of DAC and TSA. This is the first report indicating that aberrant DNA methylation and histone modifications work together to silence the sFRP2 gene in RCC cells. © 2008 Wiley-Liss, Inc. [source] Non-natural CBP2 binding peptides and peptomers modulate carcinoma cell adhesion and invasionJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 1 2001Carla Hebert Abstract A combinatorial approach that utilized a repertoire of bacteriophage-peptides has identified a number of non-natural CBP2 binding peptides. Moreover, co-localization of some of these peptides with CBP2 in a number of tumor cell lines demonstrated that the peptides were directed to an intracellular location spatially coincident with the normal distribution of CBP2 [Sauk et al., 2000]. From among these sequences WHYPWFQNWAMA and LDSRYSLQAAMY were the most effective CBP2 binding peptides and best fulfilled the combinatorial motif containing deep hydrophobic pockets. When the hydropathic profiles of collagen ,1(IV) and ,2 (IV) were compared with these dodecapeptides, the hydropathic profiles of WHYPWFQNWAMA and LDSRYSLQAAMY closely matched those of ,1(IV) 414,452 and ,1(IV)531,543. These peptides were shown to be functional peptidomimics and possessed the ability to alter cell adhesion and invasion of human squamous cell carcinoma cell lines. Peptomers were formed of these non-natural peptides to explore the role that a repetitive peptide may have on cell adhesion. The enhanced cell adhesion observed with the peptomers required both CBP2 antibodies and integrin antibodies for inhibition. The enhanced adhesion observed even in the face of combined antibody inhibition was consistent with such complexes possessing correspondingly slower dissociation rates. Thus, suggesting that peptomers may function in a like manner to multimeric peptide MHC complexes (tetramers) binding more than one cell receptor on a specific cell. These findings evoke both peptidomimics of native ligands and their peptomers as potential reagents by which to target tumor cells for chemotherapy, imaging, or retargeting viral vectors for gene therapy. J. Cell. Biochem. 82: 145,154, 2001. © 2001 Wiley-Liss, Inc. [source] Inhibition of proprotein convertases: Approaches to block squamous carcinoma development and progressionMOLECULAR CARCINOGENESIS, Issue 8 2007Ricardo López de Cicco Abstract Most proprotein convertase (PC) inhibitors are compounds that act as competitive inhibitors. All of them contain the general cleavage motif RXK/RR that binds to the PC's active site impairing further interactions with their physiological substrates. The first inhibitors synthesized were the acyl-peptidyl-chloromethyl ketones that bind to the PC's active site through its peptidyl group and are able to transverse the plasma membrane due to the acyl moiety. For instance, one of the members of this family that exhibits reduced toxicity and has been widely used as an effective general PCs inhbitor is the derivative decanoyl-RVKR-chloromethylketone (CMK). Another approach to PC inhibition is based on proteins that contain either a natural or a bioengineered PC cleavage consensus site. In this context, the bioengineered serpin, alpha-1-antitrypsin Portland (alpha 1-PDX or PDX), proved to be a potent inhibitor of furin, the most studied of the cancer-related PCs. Both PDX and CMK were able to inhibit invasiveness of squamous cell carcinoma cell lines by blocking activation of cancer-associated PC substrates such as MT-MMPs, IGF-1R, and VEGF-C. A similar effect was produced by inhibiting PC-mediated processing using furin prosegment. PDX and CMK have also been assayed in vivo using skin carcinogenesis models. Newer promising small molecules and RNA interference approaches are also being developed to inhibit PCs. © 2007 Wiley-Liss, Inc. [source] Establishment and characterization of three new rat renal cell carcinoma cell lines from N -ethyl- N -hydroxyethylnitrosamine-induced basophilic cell tumorsPATHOLOGY INTERNATIONAL, Issue 2 2001Reiko Tokuzen Three new rat cell lines (designated as BP13, BP30 and BP36B), derived from rat basophilic-type renal cell carcinomas induced with N -ethyl- N -hydroxyethylnitrosamine, were established and characterized. Passaged up to 100 times in vitro for 3 years, each cell line forms epithelial monolayers with cell cycles for BP13, BP30 and BP36B of 29, 21 and 17 h, respectively. Positive glucose-6-phosphate dehydrogenase (G6PD) and ,-glutamyltransferase (,-GT) activity in their cytoplasm, but negative succinate dehydrogenase (SD) and slightly positive carbonic anhydrase type II (CA) localization indicates an origin from proximal tubules. Ultrastructural examination showed the presence of variable numbers of mitochondria and many microvilli and intracellular junctions on the plasma membrane. BP13 and BP30 were found to be tetraploid and BP36B diploid. BP13 has one marker chromosome 15p+, and BP36B an isochromosome of 1q. Anchorage-independent growth and tumorigenicity in immunosuppressed nude mice of BP13 and BP36B, but not BP30, proved their neoplastic nature. These three cell lines should provide useful tools for studying the biological characteristics of renal cell tumors. [source] EGFR Regulates the Side Population in Head and Neck Squamous Cell CarcinomaTHE LARYNGOSCOPE, Issue 3 2006Jocelyn S. Chen BS Abstract Objective: To identify the presence of side population (SP) cells in established head and neck squamous carcinoma cell (HNSCC) lines and to determine the role of EGFR in the regulation of the side population of these cells. Methods: SP cells were identified using flow cytometry analysis by the ability of these cells to extrude the Hoechst 33342 dye via the drug transporter BCRP1/ABCG2. Effect of EGFR on the side population was determined also by difference in Hoechst extrusion and by immunofluorescence. Immunohistochemical staining was performed to show the presence of the BCRP1/ABCG2 transporter and the phosphorylated form of EGFR in HNSCC tissue. Results: SP cells are present in HNSCC cell lines. With the Hoechst 33342 extrusion assay, SP cells were found to comprise an average of 0.69% of the UMSCC10B cells and 0.91% of HN12 cells. Addition of the EGF ligand increased the SP population while inactivation of the EGFR kinase by Iressa significantly decreased SP. Conclusion: In established head and neck squamous cell carcinoma cell lines, SP cells were found using methods that determine expression and function of the drug transporter BCRP1/ABCG2. Activation of EGFR, a gene implicated in tumorigenesis in HNSCC leads to increased SP, and conversely, inhibition of EGFR leads to decrease in SP. This finding could help explain the role of EGFR in regulating cancer stem cells and thus tumorigenesis in HNSCC. [source] Establishment and characterization of seven human renal cell carcinoma cell linesBJU INTERNATIONAL, Issue 1 2000K.-H. Shin Objective,To establish human renal cell carcinoma (RCC) cell lines, and to investigate the cell phenotypes and molecular characteristics of human RCC cell lines and their corresponding tumour tissues. Materials and methods,Seven human RCC cell lines from pathologically proven RCCs were established. The histopathology of the primary tumours, in vitro growth characteristics and status of tumour suppressor genes, mismatch repair genes and microsatellite instability (MSI) were examined in cell lines and their corresponding tumour tissues. Five of the cell lines were derived from clear cells (SNU-228, -267, -328, -349, and -1272), one from granular cells (SNU-482), and one from mixed clear and granular cell types (SNU-333). The mutational status was compared for von Hippel-Lindau (VHL), p53, TGF-, type II receptor (TGF-,RII), hMSH2, and hMLH1 genes in the cell lines and their corresponding tumour tissues. The MSI status of the cell lines was determined by screening for adenine repeat sequences, e.g. BAT-25, BAT-26, and BAT-40. Results,All lines showed different doubling times and were confirmed by DNA fingerprinting analysis to be unique. Contamination by mycoplasma or bacteria was excluded. In two cell lines (SNU-349 and -1272) and their tumour tissues, mutations in the VHL gene were found. The SNU-267 line had a frameshift mutation in the p53 gene. A missense mutation of the TGF-,RII gene was detected in the SNU-1272 line and the corresponding tissue. Analysis of the repeat sequences showed one cell line (SNU-349) to have MSI and the other six to have microsatellite stability. As MSI is a hallmark of the inactivation of mismatch repair genes, the presence of hMSH2 and hMLH1 mutations was investigated in all seven cell lines. An inactivating homozygous single base-pair deletion of the hMLH1 gene was found only in the SNU-349 cell line and corresponding tissue. Moreover, a frameshift mutation within an 8-bp polyadenine repeat present in the hMSH3 coding region was found only in the MSI cell line and tumour tissue. Conclusion,These newly established RCC cell lines should provide a useful in vitro model for studies related to human RCC. The SNU-349 cell line should be especially useful for studies of MSI and mismatch repair-defective RCCs. [source] Osteopontin is a new target molecule for ovarian clear cell carcinoma therapyCANCER SCIENCE, Issue 8 2010Motoki Matsuura Recent studies have demonstrated overexpression of osteopontin (OPN) in ovarian clear cell carcinoma. Here, we revealed the role of OPN in invasiveness in ovarian clear cell carcinoma. We used immunofluorescence analysis to detect OPN in a total of 160 patient-derived specimens. Ovarian clear cell carcinoma cell lines, RMG-1 and TOV-21G, were used to monitor changes in OPN and integrin levels, and cell invasiveness following treatment with OPN, simvastatin, and transfection with siRNA. Immunofluorescence analysis revealed statistically significant differences among the histological groups, and ovarian clear cell carcinoma expressed a strong OPN signal. The OPN receptors, alpha v and 5, and beta 1 and 3 integrins, were increased after treatment with OPN. Invasion assays indicated that OPN enhanced in vitro extracellular matrix invasion dose-dependently in ovarian clear cell carcinoma. Simvastatin significantly reduced expression of OPN and the integrins, and decreased ECM invasion. RNA interference also suppressed ECM invasion. These results suggest that down- or up-regulation of OPN is involved in carcinoma cell invasion. We thus conclude that OPN regulation could have a crucial role in ovarian clear cell carcinoma therapy. (Cancer Sci 2010) [source] Prediction of in vitro response to interferon-, in renal cell carcinoma cell linesCANCER SCIENCE, Issue 4 2007Toru Shimazui We analyzed the correlation between interferon-, (IFN,) response and gene expression profiles to predict IFN, sensitivity and identified key molecules regulating the IFN, response in renal cell carcinoma (RCC) cell lines. To classify eight RCC cell lines of the SKRC series into three subgroups according to IFN, sensitivity, that is, sensitive, resistant and intermediate group, responses to IFN, (300,3000 IU/mL) were quantified by WST-1 assay. Microarray, followed by supervised hierarchical clustering analysis, was applied to selected genes according to IFN, sensitivity. In order to find alteration of expression profiles induced by IFN,, sequential microarray analyses were performed at 3, 6, and 12 h after IFN, treatment of RCC cell lines and mRNA expression level was confirmed using quantitative real time polymerase chain reaction. According to the sequential microarray analysis between IFN,-sensitive and -resistant line, seven genes were selected as candidates for IFN,-sensitivity-related genes in RCC cell lines. Among these seven genes, we further developed a model to predict tumor inhibition with four genes, that is, adipose differentiation-related protein, microphthalmia associated transcription factor, mitochondrial tumor suppressor 1, and troponin T1 using multiple linear regression analysis (coefficient = 0.948, P = 0.0291) and validated the model using other RCC cell lines including six primary cultured RCC cells. The expression levels of the combined selected genes may provide predictive information on the IFN, response in RCC. Furthermore, the IFN, response to RCC might be modulated by regulation of the expression level of these molecules. (Cancer Sci 2007; 98: 529,534) [source] Integrative molecular characterization of head and neck cancer cell model genomesHEAD & NECK: JOURNAL FOR THE SCIENCES & SPECIALTIES OF THE HEAD AND NECK, Issue 9 2010Ivy F. L. Tsui BSc Abstract Background. Cell lines are invaluable model systems for the investigation of cancer. Knowledge of the molecular alterations that exist within cell models is required to define the mechanisms governing cellular phenotypes. Methods. Five tongue squamous cell carcinomas cell lines and 1 submaxillary salivary gland epidermoid carcinoma cell line were analyzed for copy number and mRNA expression by tiling-path DNA microarrays and Agilent Whole Human Genome Oligoarrays, respectively. Results. Integrative analysis of genetic and expression alterations revealed the molecular landscape of each cell line. Molecular results for individual cell lines and across all samples have been summarized and made available for easy reference. Conclusion. Our integrative genomic analyses have defined the DNA and RNA alterations for each individual line. These data will be useful to anyone modeling oral cancer behavior, providing a molecular context that will be useful for deciphering cell phenotypes. © 2009 Wiley Periodicals, Inc. Head Neck, 2010 [source] | ||||||||||