Is Dietary Nitrate Effective in Reducing Aerobic Glycolysis in Breast Cancer?

Author(s):  
FEBS Letters ◽  
2016 ◽  
Vol 590 (18) ◽  
pp. 3179-3187 ◽  
Author(s):  
Da-Qing Yang ◽  
Dana M. Freund ◽  
Benjamin R. E. Harris ◽  
Defeng Wang ◽  
Margot P. Cleary ◽  
...  

2020 ◽  
Author(s):  
Shoukai Zong ◽  
Wei Dai ◽  
Wencheng Fang ◽  
Xiangting Guo ◽  
Kai Wang

Abstract Objective This study aimed to investigate the effect of SIK2 on cisplatin resistance induced by aerobic glycolysis in breast cancer cells and its potential mechanism. Methods qRT-PCR and Western blot were used to detect SIK2 mRNA and protein levels. Cisplatin (DDP) resistant cell lines of breast cancer cells were established, CCK-8 was used to measure and evaluate the viability, and Transwell was used to evaluate the cell invasion capability. Flow cytometry was adopted to evaluate the apoptosis rate. The glycolysis level was evaluated by measuring glucose consumption and lactic acid production. The protein levels of p-PI3K, p- protein kinase B (Akt) and p-mTOR were determined by western blot. Results SIK2 is highly expressed in breast cancer tissues and cells compared with adjacent tissues and normal human breast epithelial cells, and has higher diagnostic value for breast cancer. Silencing SIK2 expression can inhibit proliferation and invasion of breast cancer cells and induce their apoptosis. In addition, SIK2 knockdown inhibits glycolysis, reverses the resistance of drug-resistant cells to cisplatin, and inhibits PI3K/AKT/mTOR signaling pathway. When LY294002 is used to inhibit PI3K/AKT/mTOR signaling pathway, the effect of Sh-SIK2 on aerobic glycolysis of breast cancer cells can be reversed. Conclusion SIK2 can promote cisplatin resistance caused by aerobic glycolysis of breast cancer cells through PI3K/AKT/mTOR signaling pathway, which may be a new target to improve cisplatin resistance of breast cancer cells.


Oncogene ◽  
2019 ◽  
Vol 38 (28) ◽  
pp. 5551-5565 ◽  
Author(s):  
Mengjia He ◽  
Qianni Jin ◽  
Cong Chen ◽  
Yifeng Liu ◽  
Xiangsen Ye ◽  
...  

PLoS ONE ◽  
2015 ◽  
Vol 10 (7) ◽  
pp. e0132285 ◽  
Author(s):  
Yu Mi Woo ◽  
Yubin Shin ◽  
Eun Ji Lee ◽  
Sunyoung Lee ◽  
Seung Hun Jeong ◽  
...  

2002 ◽  
Vol 364 (1) ◽  
pp. 309-315 ◽  
Author(s):  
Michael GUPPY ◽  
Peter LEEDMAN ◽  
XinLin ZU ◽  
Victoria RUSSELL

For the past 70 years the dominant perception of cancer metabolism has been that it is fuelled mainly by glucose (via aerobic glycolysis) and glutamine. Consequently, investigations into the diagnosis, treatment and the basic metabolism of cancer cells have been directed by this perception. However, the data on cancer metabolism are equivocal, and in this study we have sought to clarify the issue. Using an innovative system we have measured the total ATP turnover of the MCF-7 breast cancer cell line, the contributions to this turnover by oxidative and glycolytic ATP production and the contributions to the oxidative component by glucose, lactate, glutamine, palmitate and oleate. The total ATP turnover over approx. 5days was 26.8μmol of ATP·107 cells−1·h−1. ATP production was 80% oxidative and 20% glycolytic. Contributions to the oxidative component were approx. 10% glucose, 14% glutamine, 7% palmitate, 4% oleate and 65% from unidentified sources. The contribution by glucose (glycolysis and oxidation) to total ATP turnover was 28.8%, glutamine contributed 10.7% and glucose and glutamine combined contributed 40%. Glucose and glutamine are significant fuels, but they account for less than half of the total ATP turnover. The contribution of aerobic glycolysis is not different from that in a variety of other non-transformed cell types.


2018 ◽  
pp. canres.3018.2017 ◽  
Author(s):  
Daniele Avanzato ◽  
Emanuela Pupo ◽  
Nadia Ducano ◽  
Claudio Isella ◽  
Giovanni Bertalot ◽  
...  

2019 ◽  
Vol 22 (5) ◽  
pp. 631-646 ◽  
Author(s):  
Z. Wu ◽  
J. Wu ◽  
Q. Zhao ◽  
S. Fu ◽  
J. Jin

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