Study of Apoptosis Induced by 188Re-DTPA-DG in MCF-7 Breast Carcinoma and A549 Pulmonary Carcinoma Cells

2007 ◽  
Vol 22 (4) ◽  
pp. 543-550 ◽  
Author(s):  
Qing-Feng Xiong ◽  
Yue Chen ◽  
Ling He ◽  
Cun-Liang Deng ◽  
Zhan-Wen Huang ◽  
...  
Keyword(s):  
Breast Carcinoma ◽  
Carcinoma Cells ◽  
Pulmonary Carcinoma ◽  
Mcf 7

ChemInform Abstract: Substituted Benzopyranobenzothiazinones. Synthesis and Estrogenic Activity on MCF-7 Breast Carcinoma Cells.

ChemInform ◽  
2010 ◽  
Vol 32 (35) ◽  
pp. no-no ◽  
Author(s):  
Yves Jacquot ◽  
Laurent Bermont ◽  
Herve Giorgi ◽  
Bernard Refouvelet ◽  
Gerard L. Adessi ◽  
...  
Keyword(s):  
Breast Carcinoma ◽  
Estrogenic Activity ◽  
Carcinoma Cells ◽  
Breast Carcinoma Cells ◽  
Mcf 7

scholarly journals Down-Regulation of Store-Operated Ca2+ Entry and Na+ Ca2+ Exchange in MCF-7 Breast Cancer Cells by Pharmacological JAK3 Inhibition

2016 ◽  
Vol 38 (4) ◽  
pp. 1643-1651 ◽  
Author(s):  
Jing Yan ◽  
Bingbing Zhang ◽  
Zohreh Hosseinzadeh ◽  
Florian Lang
Keyword(s):  
Breast Carcinoma ◽  
Breast Cancer Cells ◽  
Carcinoma Cells ◽  
Rt Pcr ◽  
Transcript Levels ◽  
Breast Carcinoma Cells ◽  
Store Depletion ◽  
Jak3 Inhibitor ◽  
Channel Unit ◽  
Mcf 7

Background/Aims: Oscillations of cytosolic Ca2+ activity ([Ca2+]i) participate in the orchestration of tumor cell proliferation. [Ca2+]i could be increased by intracellular Ca2+ release followed by store-operated Ca2+-entry (SOCE). [Ca2+]i could be decreased by Ca2+ extrusion via Na+/Ca2+ exchange. Mechanisms accomplishing SOCE include the pore-forming ion channel unit Orai1 and its regulator STIM1, Na+/Ca2+ exchanger isoforms include NCX1. In MCF-7 breast carcinoma cells Orai1 and NCX1 have previously been shown to be modified by pharmacological inhibition of Janus activated kinase JAK2. The present study explored whether SOCE and Na+/Ca2+ exchange are similarly sensitive to pharmacological JAK3 inhibition. Methods: MCF-7 breast carcinoma cells were studied in the absence and presence of the JAK3 inhibitor WHI-P154 (22 µM). [Ca2+]i was estimated from Fura-2-fluorescence, SOCE from increase of [Ca2+]i following Ca2+ re-addition after Ca2+-store depletion with sarcoendoplasmatic Ca2+-ATPase (SERCA) inhibitor thapsigargin (1 µM), and Na+/Ca2+ exchanger activity from increase of [Ca2+]i following extracellular Na+ removal. Transcript levels were quantified with RT-PCR. Results: Addition of ATP (100 µM) was followed by a rapid increase of [Ca2+]i, which was significantly blunted by WHI-P154. Thapsigargin-induced intracellular Ca2+ release was not appreciably influenced by WHI-P154. Subsequent SOCE was, however, significantly blunted by WHI-P154. WHI-P154 further significantly decreased Orai1 transcript levels. The increase of [Ca2+]i following extracellular Na+-removal and the NCX1 transcript levels were similarly decreased by WHI-P154. Conclusions: The JAK3 inhibitor WHI-P154 decreases both, Orai1 and NCX1 transcript levels and thus impairs SOCE and Na+/Ca2+ exchange.

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