Inhibitory Effect of Camel Urine on Neoplastic and Transformed Cell Lines

2013 ◽  
Vol 8 (2) ◽  
pp. 31-35 ◽  
Author(s):  
Mohammed M. F. Al-Halbosiy ◽  
Rakad M. Kh. Al-Jumaily ◽  
Fadhel M. Lafta ◽  
Hussam M. Hassan
1999 ◽  
pp. 447-451 ◽  
Author(s):  
F Trapasso ◽  
R Iuliano ◽  
E Chiefari ◽  
F Arturi ◽  
A Stella ◽  
...  

OBJECTIVE: Decrease or loss of the Na+/I- symporter (NIS) activity profoundly affects the suitability of the use of radioiodine to detect or treat metastatic thyroid tissues. The aim of our study was to verify whether specific oncogene abnormalities were responsible for the alteration in NIS activity in thyroid cells. DESIGN AND METHODS: Expression of the NIS gene was investigated by Northern blot analysis in normal and in some oncogene-transformed cell lines with different degrees of malignancy which had lost the iodide uptake ability. RESULTS: NIS gene expression was up-regulated by TSH in a dose-dependent and time-dependent way in normal PC Cl 3 cells. The same effect was observed by activating the cAMP-dependent pathway by forskolin. Conversely, insulin and 12-O-tetradecanoylphorbol-13-acetate (TPA) showed a partial inhibitory effect on NIS gene expression. The oncogene-transformed cell lines PC v-erbA, PC HaMSV, PC v-raf, and PC E1A cells showed reduced NIS mRNA levels compared with the normal PC Cl 3 cells. Conversely, an almost complete absence of NIS gene expression was found in PC RET/PTC, PC KiMSV, PC p53(143ala), and PC PyMLV cell lines. CONCLUSIONS: Our data show that oncogene activation could play a role in affecting the iodide uptake ability in thyroid tumoral cells; different mechanisms are involved in the oncogene-dependent loss of NIS activity in transformed thyroid cells.


1979 ◽  
Vol 43 (7) ◽  
pp. 1553-1561 ◽  
Author(s):  
Kenji KOHNO ◽  
Akiyoshi HIRAGUN ◽  
Hiromi MITSUI ◽  
Akira TAKATSUKI ◽  
Gakuzo TAMURA

2015 ◽  
Vol 209 (1) ◽  
pp. 73-84 ◽  
Author(s):  
Anaïs Aulas ◽  
Guillaume Caron ◽  
Christos G. Gkogkas ◽  
Nguyen-Vi Mohamed ◽  
Laurie Destroismaisons ◽  
...  

G3BP1, a target of TDP-43, is required for normal stress granule (SG) assembly, but the functional consequences of failed SG assembly remain unknown. Here, using both transformed cell lines and primary neurons, we investigated the functional impact of this disruption in SG dynamics. While stress-induced translational repression and recruitment of key SG proteins was undisturbed, depletion of G3BP1 or its upstream regulator TDP-43 disturbed normal interactions between SGs and processing bodies (PBs). This was concomitant with decreased SG size, reduced SG–PB docking, and impaired preservation of polyadenylated mRNA. Reintroduction of G3BP1 alone was sufficient to rescue all of these phenotypes, indicating that G3BP1 is essential for normal SG–PB interactions and SG function.


1977 ◽  
Vol 54 (4) ◽  
pp. 307-315 ◽  
Author(s):  
G. Hashiro ◽  
P. C. Loh ◽  
Jenny T. Yau

1991 ◽  
Vol 88 (9) ◽  
pp. 3792-3796 ◽  
Author(s):  
R. A. Cruciani ◽  
J. L. Barker ◽  
M. Zasloff ◽  
H. C. Chen ◽  
O. Colamonici

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