Related Experiment Video
Updated: May 12, 2026
10:33
Molecular Profiling of the Invasive Tumor Microenvironment in a 3-Dimensional Model of Colorectal Cancer Cells and Ex vivo Fibroblasts
Published on: April 29, 2014
11.4K
Gene Expression-Based Inference of Metabolic Signatures Reveals Distinct Molecular Profiles in Right- and Left-Sided
Ismail Ertuğrul1, Ayşe Büşranur Çelik2,3, Mervenur Al4
1Department of General Surgery, Kartal Dr. Lutfi Kırdar City Hospital, 34865 Istanbul, Turkey.
Metabolites
|December 24, 2025
Summary
This study reveals distinct molecular profiles in right- and left-sided colon cancers, identifying key signaling pathways and metabolites. These differences in angiogenesis, apoptosis, and metabolism may guide future colon cancer therapeutic strategies.
Area of Science:
- Oncology
- Molecular Biology
- Metabolomics
Background:
- Colon cancer is a leading global cancer, anatomically classified into right- and left-sided tumors.
- Understanding molecular distinctions between these subtypes is crucial for targeted therapies.
Purpose of the Study:
- To investigate the molecular differences between right-sided and left-sided colon cancer patients.
- To identify distinct molecular profiles, including signaling pathways and gene-metabolite interactions.
Main Methods:
- Pilot study analyzing blood samples from 6 right-sided colon cancer patients, 6 left-sided colon cancer patients, and 6 healthy controls.
- RT-qPCR analysis of 92 cancer-related genes, followed by KEGG pathway analysis and gene-metabolite interaction assessment using bioinformatics tools.
Main Results:
- Right-sided colon cancer showed enrichment in p53, HIF-1, TNF, PI3K/Akt, MAPK, and Rap1 signaling pathways.
- Left-sided colon cancer implicated VEGF, HIF-1, MAPK, PI3K/Akt, Rap1, and Ras signaling pathways.
- Distinct gene-metabolite networks identified, with key metabolites like palmitic acid and glucose-6-phosphate linked to specific genes in each subtype.
Conclusions:
- Significant molecular differences exist between right- and left-sided colon cancers.
- These disparities involve pathways critical for angiogenesis, apoptosis, ferroptosis, and fatty acid metabolism.
- Findings may pave the way for novel, subtype-specific therapeutic interventions for colon cancer.
Related Concept Videos
02:18Cancer
Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.
02:07Tumor Progression
Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
01:33Cancer-Critical Genes I: Proto-oncogenes
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
01:05Cancer-Critical Genes II: Tumor Suppressor Genes
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
01:05Cancer-Critical Genes II: Tumor Suppressor Genes
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
01:11Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...