scholarly journals Evaluation of the anti-tumor activities of Sulfonylurea Derivatives

2022 ◽  
Sha Zhou ◽  
Sen Lu ◽  
Chenchen Guo ◽  
Lei Wu ◽  
Zhanying Zheng ◽  

This study prepared 25 sulfonylurea compounds to evaluate anti-tumor activity. Through experimental investigations in MDA-MB-231 and MCF-7, i.e., cell lines of breast carcinoma of human, we have concluded that some compounds can significantly suppress breast carcinoma cells from growing and proliferating. Moreover, the compound M’s inhibitory effect on cells of breast carcinoma is concentration-dependent under a certain treatment time; and the inhibitory effect of the compound M on breast carcinoma cells is time-dependent under a certain concentration. In addition, we also found that the compound M can effectively suppress cells of breast carcinoma from migration and independent survival. The results can show the prospect of research and development of new breast carcinoma treatment drug.

ChemInform ◽  
2010 ◽  
Vol 32 (35) ◽  
pp. no-no ◽  
Yves Jacquot ◽  
Laurent Bermont ◽  
Herve Giorgi ◽  
Bernard Refouvelet ◽  
Gerard L. Adessi ◽  

2016 ◽  
Vol 38 (4) ◽  
pp. 1643-1651 ◽  
Jing Yan ◽  
Bingbing Zhang ◽  
Zohreh Hosseinzadeh ◽  
Florian Lang

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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