Disease relevance of TPCN1

• We then compared the biological effects of IL-4 in TPC-1, a thyroid cancer cell line, and in MCF-7 breast cancer cells [1].
• All of the four transcripts in TPC-1 are about 2 kb smaller than the corresponding ones in the neuroblastoma [2].
• Nuclear extracts from the well differentiated TPC-1 (from papillary carcinoma) and the poorly differentiated ARO (from anaplastic carcinoma) cells showed an overall similar pattern of protein expression as revealed by two-dimensional gel electrophoresis analysis [3].
• A generalized transducing thiophage (TPC-1) of a facultative sulfur chemolithotrophic bacterium, Bosea thiooxidans CT5, of alpha-Proteobacteria, isolated from Indian soil [4].
• We have isolated and characterized a double-stranded DNA bacteriophage (TPC-1) of Bosea thiooxidans, a facultative sulfur chemolithotrophic bacterium [4].

High impact information on TPCN1

• Genomic breakpoints from a PC and a PC cell line (TPC-1) were cloned and sequenced [5].
• TPC1 cells were more sensitive to growth inhibition (IC50 0.1-0.25 and approximately 0.05 micromol/L for AAL-881 and LBT-613, respectively) than BRAF + lines (IC50 2.5-5 and 0.1-0.5 micromol/L, respectively) [6].
• After 6 d of treatment with 50 nM geldanamycin, the percent inhibition of growth was 29.4% in TPC-1, 97.5% in FTC-133, 96.7% in FTC-236, 10.8% in FTC-238, 70.9% in XTC-1, and 45.5% in ARO cell lines [7].
• Thyroid cancer cell lines (XTC-1 > TPC-1 > FTC-133 > MTC-1.1) also secreted more VEGF protein as measured by ELISA than did normal thyroid cells [8].
• Down-regulation of thyroid-specific transcription factor-1 expression was observed in BCPAP and TPC-1 cell lines [9].

Chemical compound and disease context of TPCN1

• TPC-1 is classified as the C1 morphotype of the Podoviridae family [4].
• PTC mRNA was detected by the RT-PCR method in only one papillary carcinoma cell line (TPC-1 cell) [10].

Biological context of TPCN1

• Deletion of the H4 gene on the chromosome 10 not involved in the t(1; 10; 21) translocation suggests lack of normal H4 expression in the TPC-1 cell line [11].
• On the other hand, it did not induce a significant change in cell shape of TPC-1 cells [12].
• Hybridization to TPC-1 interphase nuclei showed one yellow domain, and 1 red and 1 green domain separated by a large physical distance [11].
• In a papillary thyroid carcinoma cell line, TPC-1, we found transcripts hybridizing to ret proto-oncogene (proto-ret) cDNA probes [2].
• In both TPC-1 (TRAIL-sensitive) and FTC-133 (TRAIL-resistant) thyroid cancer cell lines, pretreatment with troglitazone, cycloheximide, and paclitaxel enhanced TRAIL-induced cell death significantly but pretreatment with geldanamycin did not [13].

Anatomical context of TPCN1

• In the thyroid tumor cell lines TPC-1 and B-CPAP, APE/Ref-1 was not effective by itself, and it also failed to increase PAX8 stimulation on NIS promoter activity [14].
• We used six thyroid cancer cell lines: TPC-1, FTC-133, FTC-236, FTC-238, XTC-1, and ARO82-1 [13].
• DNA from individual clones representing the respective ends of a yeast artificial chromosome (YAC) contig spanning the entire ret gene locus were labeled with either digoxigenin (visualized in red) or biotin (green) and hybridized to normal human lymphocytes and the papillary thyroid cancer cell line TPC-1 expressing the ret/H4 chimeric transcript [11].
• TPC-1 cell line exhibited a three-dimensional structure of transitional epithelium on the nylon-mesh disk which was coated with a layer of rat tail collagen [15].
• The second cell line derived from the urothelium of a papillocarcinoma in the left renal pelvis was designated as TPC-1 and grown in vitro for more than 100 generations [15].

Associations of TPCN1 with chemical compounds

• By this sensitive method retTPC/PTC transcript could be detected in about 500 fg of total RNA of TPC-1, a retTPC/PTC transcript-positive cell line [16].
• We examined the effect of herbimycin A, a potent inhibitor of tyrosine kinases, on NIH(ret) cells and TPC-1 papillary thyroid carcinoma cells, both of which express the active ret genes [12].
• When tyrosine kinase activities of the active ret gene products in herbimycin A-treated NIH(ret) and TPC-1 cells were examined in immunocomplex kinase assays, they drastically decreased in both cells as compared with untreated cells [12].
• Administration of ZD6474 led to an up to 95% reduction of cell number in Hth74, 85% in C643, 90% in FTC133, and 90% in TPC1 (p < 0.05) [17].
• Administration of ZD1839 led to an up to 90% reduction of cell number in Hth74, 80% in C643, 50% in FTC133, and 90% in TPC1 (p < 0.05) [17].

Regulatory relationships of TPCN1

• IL-8 was also produced at high levels in TT human medullary thyroid carcinoma and TPC-1 human papillary thyroid carcinoma cell lines both of which express activated RET tyrosine kinase [18].

Other interactions of TPCN1

• In our study, the proliferation of TPC-1, the papillary thyroid carcinoma cell line, was reduced by both recombinant ActA and TGF-beta1 [19].
• Finally, we applied our FISH approach to determine the extent of deletion involving this locus (D10S170) in a papillary thyroid cancer cell line, TPC-1 [20].
• Thyroid-specific transcription factor-2 mRNA was reduced in FRO, BCPAP, and TPC-1 cells [9].
• Incubation with tissue plasminogen activator (TPA), an agonist of PKC, of two papillary (NPA and TPC-1) and one anaplastic (ARO) carcinoma cell lines induced an ICAM-1 upregulation of both protein and mRNA production [21].
• TPO expression is lost in several thyroid carcinoma cell lines (TPC-1, 8305C, 8505C) and altered in another (TC-80) [22].

Analytical, diagnostic and therapeutic context of TPCN1

• Northern blot analysis showed that TPC1 mRNA (5 kb) was expressed widely [23].
• Immunohistochemistry of kidney revealed that TPC1 was expressed at inner medullary collecting ducts [23].
• The effects of BAY 43-9006 on proliferation of human TPC1 and TT thyroid carcinoma cells, which harbor spontaneous oncogenic RET alleles, and on RAT1 fibroblasts transformed with oncogenic RET mutants, including mutants that are resistant to other chemotherapeutic agents, were determined using growth curves and flow cytometry [24].

References