Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Out of seven human carcinoma cell lines (M7609, CCK-81, FCC-1, RPMI#4788, QGP-1, HLC-1, and KNS-62), 4 cell lines were found to produce immunoreactive calcitonin (ICT), a potential tumor marker for various malignancies. During a 7-day culture, 1.4 X 10(5) QGP-1, RPMI#4788, HLC-1, and KNS-62 cells secreted 7,000 pg, 500 pg, 400 pg, and 400 pg of ICT in the medium, respectively. The production of ICT by QGP-1 cells was increased by addition of pentagastrin or calcium gluconate. Three different components of ICT (peak I, molecular weight greater than 40,000; peak II, 14,000-18,000; peak III, 3,400) were detected by gel filtration of the QGP-1 spent medium. In a competitive inhibition-type radioimmunoassay of serial dilutions of each ICT component, peak III component showed very similar immunoreactivity to synthetic calcitonin. However, the other two components gave clearly different immunoreactivities from the peak III component and showed very similar immunoreactivities to each other. All the cell lines were further screened for synthesis of 7 other tumor markers, carcinoembryonic antigen, nonspecific cross-reacting antigen, CA19-9, tissue polypeptide antigen, alpha-fetoprotein, beta 2-microglobulin and ferritin. Every cell line produced 2 to 6 markers concomitantly, and various combinations of positive markers were found among the cell lines.
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PMID:Production of immunoreactive calcitonin and some other tumor markers by established human carcinoma cell lines. 308 16

Early diagnosis of lung cancer by non-invasive methods has a low sensibility: 60% of peripheral cancers could be diagnosed by computed tomography, 60% of the central ones by sputum cytology. More specific for detecting central microinvasive lesions could be bronchoscopy with autofluorescence, but this is a method with a low number of patients to be performed on, because of the specific technique. For all these reasons there are some other methods to be tried in this respect--one of them is to find one or more molecules--tumoral markers--which have to be specific in establishing the risk of developing lung cancer, to make an early diagnosis of cancer and to predict the evolution under treatment. The detecting tumoral markers in sputum, blood, bronchoalveolar lavage was not so largely explored related to the final goal--the possibility of identifying and quantifying the most specific ones for the screening of lung cancer. The present paper has as purpose to make an review of tumoral markers--"classical" markers as: CEA, NSE, TPA, beta2 microglobulina, CA 125, CA 15-3--considered not such a high sensibility and specificity for lung cancer screening versus new molecules, studied intensively as: SCC-Ag, CYFRA 21-1, ferritin, sIL-2R, CCK-BB, glycosyltransferases. Those new molecules have a higher sensibility, but also could have a higher specificity for each type of lung cancer.
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PMID:[Update regarding the role of biomarkers in early diagnosis of non-small cell bronchopulmonary cancer]. 2154 94

VTo investigate the effect of nuclear transcription factor Nrf2 on the transcription of Ferroportin (FPN) in prostate cancer cells, and the regulation mechanisms of FPN on cell viability, migration and apoptosis of prostate cancer cells.Empty vectors, pEGFPC1-Nrf2, pEGFPC1-FPN, Si-FPN and Si-Nrf2 were transfected into prostate cancer cell line PC3. The expression of mRNA and protein were measured by real time-PCR (RT-PCR) and western blot. Cell viability, migration, cycle and apoptosis were tested by CCK-8 assay, wound healing and flow cytometry, respectively. The interaction between FPN and Nrf2 was confirmed by chromatin immunoprecipitation (CHIP) assay.The viability, migration and mitosis of PC3 cells could be repressed by over-expressed FPN, with decreased intracellular ferritin. The CHIP assay demonstrated that Nrf2 is one transcription factor of FPN and promotes its transcription. With the increase of Nrf2 in PC3 cells, the viability, migration ability and concentration of ferritin were suppressed, while the apoptosis rate was increased. The above effects were counteracted by down-regulating FPN.FPN could inhibit the prostate cancer cell viability, migration and mitosis, which is also related to a decrease of intracellular ferritin content. In conclusion, Nrf2 suppresses prostate cancer cells viability, migration, and mitosis through upregulating FPN.
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PMID:Nuclear transcription factor Nrf2 suppresses prostate cancer cells growth and migration through upregulating ferroportin. 2778 96