Leukocyte-Cancer Cell Fusion: Initiator of the Warburg Effect in Malignancy?

2011 ◽  
pp. 151-172 ◽  
Author(s):  
Rossitza Lazova ◽  
Ashok Chakraborty ◽  
John M. Pawelek
Keyword(s):  
Cell Fusion ◽  
Cancer Cell ◽  
Warburg Effect ◽  
The Warburg Effect

Glucose restriction reverses the Warburg effect and modulates PKM2 and mTOR expression in breast cancer cell lines

2019 ◽  
Vol 65 (7) ◽  
pp. 26 ◽  
Author(s):  
Roula Tahtouh ◽  
Layal Wardi ◽  
Riad Sarkis ◽  
Ray Hachem ◽  
Issam Raad ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Warburg Effect ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Glucose Restriction ◽  
The Warburg Effect

scholarly journals Alterations in cancer cell metabolism: The Warburg effect and metabolic adaptation

Genomics ◽  
2015 ◽  
Vol 105 (5-6) ◽  
pp. 275-281 ◽  
Author(s):  
Yazdan Asgari ◽  
Zahra Zabihinpour ◽  
Ali Salehzadeh-Yazdi ◽  
Falk Schreiber ◽  
Ali Masoudi-Nejad
Keyword(s):  
Cancer Cell ◽  
Warburg Effect ◽  
Cell Metabolism ◽  
Metabolic Adaptation ◽  
Cancer Cell Metabolism ◽  
The Warburg Effect

Novel glycoconjugated squaraine dyes for selective optical imaging of cancer cells

2017 ◽  
Vol 53 (39) ◽  
pp. 5433-5436 ◽  
Author(s):  
M. Shimi ◽  
Vandana Sankar ◽  
M. K. Abdul Rahim ◽  
P. R. Nitha ◽  
Suresh Das ◽  
...  
Keyword(s):  
Optical Imaging ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Warburg Effect ◽  
Cancer Cell Lines ◽  
Squaraine Dyes ◽  
Cell Selectivity ◽  
The Warburg Effect

Glycoconjugated squaraine dyes for selective internalisation in cancer cell lines are reported. The cancer cell selectivity was achieved through the “Warburg effect”.

scholarly journals Pan-Cancer Analysis of Glycolytic and Ketone Bodies Metabolic Genes: Implications for Response to Ketogenic Dietary Therapy

2021 ◽  
Vol 11 ◽  
Author(s):  
Liyuan Qian ◽  
Yunzheng Li ◽  
Yajuan Cao ◽  
Gang Meng ◽  
Jin Peng ◽  
...  
Keyword(s):  
Clinical Outcomes ◽  
Cancer Cell ◽  
Warburg Effect ◽  
Ketone Bodies ◽  
Aerobic Glycolysis ◽  
System Level ◽  
Dietary Therapy ◽  
Joint Analysis ◽  
Ketogenic Diets ◽  
The Warburg Effect

BackgroundThe Warburg effect, also termed “aerobic glycolysis”, is one of the most remarkable and ubiquitous metabolic characteristics exhibited by cancer cells, representing a potential vulnerability that might be targeted for tumor therapy. Ketogenic diets (KDs), composed of high-fat, moderate-protein and low carbohydrates, are aimed at targeting the Warburg effect for cancer treatment, which have recently gained considerable attention. However, the efficiency of KDs was inconsistent, and the genotypic contribution is still largely unknown.MethodsThe bulk RNA-seq data from The Cancer Genome Atlas (TCGA), single cell RNA sequencing (scRNA-seq), and microarray data from Gene Expression Omnibus (GEO) and Cancer Cell Line Encyclopedia (CCLE) were collected. A joint analysis of glycolysis and ketone bodies metabolism (KBM) pathway was performed across over 10,000 tumor samples and nearly 1,000 cancer cell lines. A series of bioinformatic approaches were combined to identify a metabolic subtype that may predict the response to ketogenic dietary therapy (KDT). Mouse xenografts were established to validate the predictive utility of our subtypes in response to KDT.ResultsWe first provided a system-level view of the expression pattern and prognosis of the signature genes from glycolysis and KBM pathway across 33 cancer types. Analysis by joint stratification of glycolysis and KBM revealed four metabolic subtypes, which correlated extensively but diversely with clinical outcomes across cancers. The glycolytic subtypes may be driven by TP53 mutations, whereas the KB-metabolic subtypes may be mediated by CTNNB1 (β-catenin) mutations. The glycolytic subtypes may have a better response to KDs compared to the other three subtypes. We preliminarily confirmed the idea by literature review and further performed a proof-of-concept experiment to validate the predictive value of the metabolic subtype in liver cancer xenografts.ConclusionsOur findings identified a metabolic subtype based on glycolysis and KBM that may serve as a promising biomarker to predict the clinical outcomes and therapeutic responses to KDT.

scholarly journals Inverse correlation between heme synthesis and the Warburg effect in cancer cells

2019 ◽  
Author(s):  
Yuta Sugiyama ◽  
Erika Takahashi ◽  
Kiwamu Takahashi ◽  
Motowo Nakajima ◽  
Tohru Tanaka ◽  
...  
Keyword(s):  
Electron Transfer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Warburg Effect ◽  
Metabolic Adaptation ◽  
Human Gastric Cancer ◽  
Transfer System ◽  
Heme Synthesis ◽  
Electron Transfer System ◽  
The Warburg Effect

AbstractsCancer cells show a bias toward the glycolytic system over the conventional mitochondrial electron transfer system for obtaining energy. This biased metabolic adaptation is called the Warburg effect. Cancer cells also exhibit a characteristic metabolism, a decreased heme synthesizing ability. Here we show that heme synthesis and the Warburg effect are inversely correlated. We used human gastric cancer cell lines to investigate glycolytic metabolism and electron transfer system toward promotion/inhibition of heme synthesis. Under hypoxic conditions, heme synthesis was suppressed and the glycolytic system was enhanced. Addition of a heme precursor for the promotion of heme synthesis led to an enhanced electron transfer system and inhibited the glycolytic system and vice versa. Enhanced heme synthesis leads to suppression of cancer cell proliferation by increasing intracellular reactive oxygen species levels. Collectively, the promotion of heme synthesis in cancer cells eliminated the Warburg effect by shifting energy metabolism from glycolysis to oxidative phosphorylation.

scholarly journals Protein Phosphatase 2A Inhibits Gastric Cancer Cell Glycolysis by Reducing MYC Signaling

2021 ◽  
Author(s):  
Wei Zhang ◽  
Zhenhua Cai ◽  
Ruiqing Zhou ◽  
Xiaohui Liu ◽  
Yuhong Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Protein Phosphatase ◽  
Warburg Effect ◽  
Gastric Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Pp2a Activity ◽  
Gastric Cancer Cell Proliferation ◽  
The Warburg Effect

Abstract Background: The Warburg effect is closely associated malignant phenotypes and poor prognosis in cancer patients. PP2A is a highly conserved eukaryotic serine/threonine protein phosphatase that functions as a tumor suppressor in a variety of human cancers. However, the relationship between PP2A and the Warburg effect has yet to be fully understood. Methods: The expression profile of two endogenous inhibitors of PP2A, SET and CIP2A, are detected by real-time qPCR. Loss-of-function and gain-of-function are performed to demonstrate the roles of PP2A in gastric cancer cell proliferation and glycolysis. Cell biological, molecular, and biochemical approaches are used to uncover the underlying mechanism. Results: In this study, we find that SET and CIP2A are overexpressed in gastric cancer and associates a decreased PP2A activity. Pharmacological activation of PP2A with FTY-720 and DT-061 significantly reduces gastric cancer cell proliferation and glycolytic ability. Importantly, inhibition of PP2A activity by genetic silencing of PPP2R5A induces a growth advantage, which can be largely compromised by addition of the glycolysis inhibitor 2-Deoxy-D-glucose, suggesting a glycolysis-dependent effect of PP2A in gastric cancer. Mechanistically, the well known transcription factor and glycolysis regulator c-Myc is discovered as the functional mediator of PP2A in regulating cell glycolysis. Ectopic expression of a phosphorylation-mutant c-Myc resistant to PP2A (MycT58A) restores the inhibitory effect of FTY-720 and DT-061 on the lactate production and glucose uptake. Furthermore, there is a close association between SET and CIP2A expression and c-Myc gene signatures in gastric cancer samples. Conclusions: This study provides strong evidence of the involvement of PP2A in the Warburg effect and indicates that it could be a novel antitumor strategy to target tumor metabolism in gastric cancer.

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