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The mechanisms by which TXNIP is expressed and functions in thyroid cancer will improve our understanding of the progression to advanced thyroid cancer and help to develop more effective targeted therapies.MethodsCell lines and maintenanceConclusions In conclusion, we report that TXNIP is a novel tumor suppressor in thyroid cancer. TXNIP is downregulated during the progression from well-differenti
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D drastically diminished pulmonary metastatic tumor burden. These data highlight the importance of TXNIP as a potential therapeutic target and prognostic marker in advanced thyroid cancer.HTh74 and C643 cells were obtained from Dr. K. Ain (University of Kentucky, Lexington, KY) with permission from N. E. Heldin (University Hospital, Uppsala, Sweden). TPC1 cells were provided by S. Jhiang (Ohio Sta
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Gnosis and increased mortality [49,50]. The mechanism underlying this differential glucose uptake between well-differentiated PTC and ATC is not well understood. The novel finding that TXNIP expression is low in ATC is consistent with the observed FDG uptake on PET/CT in patients with ATC, supporting a critical role for TXNIP as a metabolic regulator in thyroid cancer progression. In addition to i
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Promoting a pro-apoptotic environment [13,15-20]. Independent of its interaction with thioredoxin, TXNIP also has the ability to inhibit cell cycle progression by indirectly stabilizing the cell cycle inhibitor p27Kip1 [9]. In addition, TXNIPMorrison et al. Molecular Cancer 2014, 13:62 http://www.molecular-cancer.com/content/13/1/Page 8 ofAvectorB*** *TXNIPCD******Figure 5 TXNIP overexpression in
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Our prior studies using HTh74 cells in the orthotopic murine thyroid cancer model system, we have observed that the in vivo growth rates are slower compared to other thyroid cancer cell lines (84 days to achieve 100 mm3 tumors compared with 28?5 days in other ATC cell lines). It is possible that if our study had been temporally extended, the trend in tumor volume attenuation in the TXNIP-overexpre
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Gnosis and increased mortality [49,50]. The mechanism underlying this differential glucose uptake between well-differentiated PTC and ATC is not well understood. The novel finding that TXNIP expression is low in ATC is consistent with the observed FDG uptake on PET/CT in patients with ATC, supporting a critical role for TXNIP as a metabolic regulator in thyroid cancer progression. In addition to i
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Uares () indicate vector control cells, and open diamonds () indicate cells with TXNIP overexpression. In vitro invasion assays were performed on the TXNIP-overexpressing stable HTh74 (C) and T238 (D) cell lines as described in the Methods section. Results from three independent experiments were combined and normalized to the vector control average and graphed with mean plus SEM. *p
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Uares () indicate vector control cells, and open diamonds () indicate cells with TXNIP overexpression. In vitro invasion assays were performed on the TXNIP-overexpressing stable HTh74 (C) and T238 (D) cell lines as described in the Methods section. Results from three independent experiments were combined and normalized to the vector control average and graphed with mean plus SEM. *p
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Uares () indicate vector control cells, and open diamonds () indicate cells with TXNIP overexpression. In vitro invasion assays were performed on the TXNIP-overexpressing stable HTh74 (C) and T238 (D) cell lines as described in the Methods section. Results from three independent experiments were combined and normalized to the vector control average and graphed with mean plus SEM. *p