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Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer

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Published on: September 18, 2020

Differences in glucose concentration shows new perspectives in gastric cancer metabolism

Emerson Lucena da Silva¹, Felipe Pantoja Mesquita¹, Adrhyann Jullyanne de Sousa Portilho¹

¹Laboratory of Pharmacogenetics, Drug Research and Development Center (NPDM), Federal University of Ceará, Cel. Nunes de Melo, 1000 - Rodolfo Teófilo, Fortaleza, Brazil.

Toxicology in Vitro : an International Journal Published in Association with BIBRA

|April 15, 2022

Abstract:

Gastric cancer (GC) is among the deadliest cancers worldwide despite available therapies, highlighting the need for novel therapies and pharmacological agents. Metabolic deregulation is a potential study area for new anticancer targets, but the in vitro metabolic studies are controversial, as different ranges of glucose used in the culture media can influence results. In this study, we evaluated cellular viability, glucose uptake, and LDH activity in gastric cancer cell lines when exposed to different glucose concentrations: high (HG, 25mM), low (LG, 5.5mM), and free (FG, 0mM) glucose media. Moreover, we evaluated how glucose variations may influence cellular phenotype and the expression of genes related to epithelial-mesenchymal transition (EMT), metabolism, and cancer development in metastatic GC cells (AGP-01). Results showed that metastatic cells exposed to FG medium evidenced higher alterations when compared to other cell lines. Most phenotypic assays did not show difference when exposed to either HG or LG media. However, gene expression profile of cells exposed to LG revealed differences in mRNA levels of metabolism-related genes when compared to HG medium. According to our results, we recommend using LG medium for metabolic studies since the glucose concentration is closer to physiological levels. These findings point out new relevant targets in metabolic reprogramming that can be alternatives to current chemotherapies in patients with metastatic GC.

Insights

This study investigated how glucose levels affect gastric cancer cells in lab cultures. Researchers recommend using low glucose media for more accurate metabolic studies in gastric cancer research.

Area of Science:

Oncology
Metabolic Research
Cell Biology

Background:

Gastric cancer (GC) remains a leading cause of cancer mortality globally.
Existing therapies are insufficient, necessitating novel treatment strategies.
In vitro metabolic studies in GC are complicated by variable glucose concentrations in culture media.

Purpose of the Study:

To assess the impact of varying glucose concentrations (high, low, free) on gastric cancer cell viability, glucose uptake, and LDH activity.
To investigate how glucose levels influence cellular phenotype and gene expression, particularly EMT and metabolism-related genes, in metastatic GC cells.
To determine optimal glucose concentrations for in vitro metabolic studies in GC.

Main Methods:

Gastric cancer cell lines were cultured in media with high (25mM), low (5.5mM), or free (0mM) glucose.
Cellular viability, glucose uptake, and lactate dehydrogenase (LDH) activity were measured.
Phenotypic assays and gene expression profiling (mRNA levels) were performed, focusing on EMT, metabolism, and cancer development markers.

Main Results:

Metastatic GC cells showed significant alterations in free glucose medium compared to other conditions.
Phenotypic assays revealed minimal differences between high and low glucose media.
Gene expression analysis indicated distinct mRNA levels of metabolism-related genes in low glucose versus high glucose conditions.

Conclusions:

Low glucose medium (5.5mM) is recommended for in vitro metabolic studies of gastric cancer due to its closer approximation to physiological glucose levels.
Metabolic reprogramming in gastric cancer presents potential therapeutic targets.
These findings may offer alternative therapeutic strategies for metastatic gastric cancer patients.

Read full analysis

Keywords:

Aerobic pathways Cancer microenvironment Gastric cancer Glucose deprivation Metabolism reprogramming

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