scholarly journals Grape seed procyanidin B2 promotes the autophagy and apoptosis in colorectal cancer cells via regulating PI3K/Akt signaling pathway [Corrigendum]

2019 ◽  
Vol Volume 12 ◽  
pp. 4665-4666
Author(s):  
Ruijuan Zhang ◽  
Qianyun Yu ◽  
Wenqiang Lu ◽  
Jun Shen ◽  
Dongqing Zhou ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Grape Seed ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Colorectal Cancer Cells

scholarly journals Grape seed procyanidin B2 promotes the autophagy and apoptosis in colorectal cancer cells via regulating PI3K/Akt signaling pathway

2019 ◽  
Vol Volume 12 ◽  
pp. 4109-4118 ◽  
Author(s):  
Ruijuan Zhang ◽  
Qianyun Yu ◽  
Wenqiang Lu ◽  
Jun Shen ◽  
Dongqing Zhou ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Grape Seed ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Colorectal Cancer Cells

scholarly journals Retraction: Daphnetin inhibits proliferation and glycolysis in colorectal cancer cells by regulating the PI3K/Akt signaling pathway

RSC Advances ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 5023-5023
Author(s):  
Laura Fisher
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Colorectal Cancer Cells

Retraction of ‘Daphnetin inhibits proliferation and glycolysis in colorectal cancer cells by regulating the PI3K/Akt signaling pathway’ by Zhikuan He et al., RSC Adv., 2018, 8, 34483–34490, DOI: 10.1039/C8RA05583A.

scholarly journals Butyrate Suppresses Glucose Metabolism of Colorectal Cancer Cells via GPR109a-AKT Signaling Pathway and Enhances Chemotherapy

2021 ◽  
Vol 8 ◽  
Author(s):  
Hong-Wei Geng ◽  
Feng-Yi Yin ◽  
Zhi-Fa Zhang ◽  
Xu Gong ◽  
Yun Yang
Keyword(s):  
Colorectal Cancer ◽  
Glucose Metabolism ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Histone Deacetylases ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Anti Cancer ◽  
Colorectal Cancer Cells ◽  
The Impact

Glycolysis inhibitors are promising therapeutic drugs for tumor treatment, which target the uniquely elevated glucose metabolism of cancer cells. Butyrate is a critical product of beneficial microbes in the colon, which exerts extraordinary anti-cancer activities. In particular, butyrate shows biased inhibitory effects on the cell growth of cancerous colonocytes, whereas it is the major energy source for normal colonocytes. Besides its roles as the histone deacetylases (HDACs) inhibitor and the ligand for G-protein coupled receptor (GPR) 109a, the influence of butyrate on the glucose metabolism of cancerous colonocytes and the underlying molecular mechanism are not fully understood. Here, we show that butyrate markedly inhibited glucose transport and glycolysis of colorectal cancer cells, through reducing the abundance of membrane GLUT1 and cytoplasmic G6PD, which was regulated by the GPR109a-AKT signaling pathway. Moreover, butyrate significantly promoted the chemotherapeutical efficacy of 5-fluorouracil (5-FU) on cancerous colonocytes, with exacerbated impairment of DNA synthesis efficiency. Our findings provide useful information to better understand the molecular basis for the impact of butyrate on the glucose metabolism of colorectal cancer cells, which would promote the development of beneficial metabolites of gut microbiota as therapeutical or adjuvant anti-cancer drugs.

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