How cancer cells interact with the body?

Home Cancer How cancer cells interact with the body?
Human body and cancer cells

Tumor progression, a primary triggering factor of cancer is influenced by genetic and epigenetic abnormality. A malignant tumor is usually aggressive in nature and progression of the malignancy clinically leads to cancer development. However, the rate of progression and time course are variable and dependable upon several biological and clinical factors. The clinical significance of malignancy can be described as neoplastic cells, which can invade locally and metastasize at distant organs and the remaining body.

Cancer affects body

The cancer cell progress from primary tumor mass to a distant organ due to loss of cellular bonding and alteration of cellular matrix. This allows the cancer cell to invade the surrounding tissues and the process is known as an invasion. The gradual interaction between surrounding tissues and tumor cell promotes angiogenesis, through which blood circulation takes place and cancer progresses. This process is known as intravasation.  The biochemical interaction which is mediated through carbohydrate locking reaction assist in interaction with endothelial cells, which is known as extravasation.

The interaction of endothelium and basement membrane initiates new tumor growth. Therefore, the whole cancer metastatic process depends upon invasion, intravasation, and extravasation.

The biochemical changes in the metabolic pathway of the malignant tumor cells often involve proteolytic enzymes, activation of plasminogen, tumor angiogenic factor, aggregation of platelet, and laminin, fibronectin is several membrane molecules production, and complex gene structure that is made up with histological compatible gene products. It influences neoplastic development and ‘oncogenes’ formation.

The process of cancer development is quite understandable after advancement of the cellular and molecular biochemistry. DNA methylation alteration is one of the basic differences between a normal cell and a cancer cell. Abnormal hypo and hypermethylation is the characteristic feature of a cancer cell, which is not found in normal cell development. Global hypomethylation, which can be hypermethylated in presence of a specific promoter is the typical characteristic of the cancer cell. Global hypomethylation activates ‘oncogenes’ and promotes mutation by providing genomic instability. Subsequently, hypermethylation inhibits the activity of tumor-suppressor genes, which provide protection to the normal cell from unwanted cell growth and progression of cancer. Researchers found that the tumor suppressor p53 has an essential role to prevent unwanted cell growth, the progression of cell cycle evolution, and cell apoptosis.  In addition, the energy production in a normal cell is restricted in mitochondria and mainly depends upon pyruvic acid oxidation. Whereas, in cancer cells, the predominant energy production is achieved through an increasing level of glycolysis in the cytosol under anaerobic conditions. In the progressive stage of cancer, DNA gets damaged due to abnormal methylation which causes restricted growth of tumor suppressor p53 and negative cellular regulatory process that influence cancer cell proliferation.

The metabolic pathway alters the energy metabolism and the biochemical changes that are obtained due to the reduction/oxidation pathway which influences DNA damage and promotes cancer. Researchers found an imbalance in redox and increased oxidative stress in cancerous tissue development. All cellular metabolic functions require oxygen to pursue the metabolic process and Reactive oxygen species (ROS) are bioproducts of these metabolic processes. A balanced level of oxidants and antioxidants in the physiological system is essential for proper cellular functioning. Redox biochemistry plays an important role in balancing these levels. However, it is well established that the imbalanced oxidant and antioxidant level due to altered redox reaction is one of the primary findings in cancers. Oxidative and /or nitrosative stress alter the biochemical property of normal cellular physiology by modulating phosphorylation, methylation, acetylation, sumoylation, nitrosylation, nitration, and glutathionylation. These consequences negatively affect oncogenes, transcription factors, tumor suppressors, and proteins that control antioxidant/prooxidant balance and the proteins that control the metabolic process.

The presence of an increased level of oxidants negatively affects protein functioning by converting −SH groups to disulfides. Two protein enzymes like transcription factors and ribonucleotide reductase play a major role in cancer development but the antioxidant protein and thioredoxin neutralize these enzyme activities by promoting redox reaction.

Redox imbalance and reduced activity of Thioredoxin is prominent in human breast and prostate cancer. Imbalance of redox state initiates an increased level of glutathione, which decreases cell apoptosis and protects chronic lymphocytic leukemia cells.

Epigenetic factors also induce biochemical changes that influence cancer progression. Epigenetic factors include intrinsic environmental or lifestyle-related changes to DNA or a chromosomal structure obtained after birth. The epigenetic alteration inducing single mutagenic changes has the potential to alter cellular biochemistry, metabolism, and cellular behavior.

Protein stability is another important factor in the biochemical alteration of cancer cell progression. Protein stability is coordinated by altering in folding or unfolding of protein molecular structure, configurationally alteration of protein structure, hydrogen bonding, hydrophobic interactions, redox potential, temperature, pH, and binding potentiality with metal.  For example, nuclear factor erythroid 2-related factor 2 (NRF2) is stable in normal cells and stimulates antioxidant genes and cytoprotective enzymes; but the instability of NRF2, which protects cancer cells from chemotherapeutic agents and radiation therapy; the results of which causes treatment failure.




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