Mitochondria in cancer

Introduction:

Organisms like rod-like, round, round or stellate vesicles scattered around the nucleus or scattered in the cytoplasm during cell division are called mitochondria (singular-mitochondrion). In 1894, Altmann observed the presence of mitochondria. But in 1897, Benda named it Mitochondrion. Mitochondria vary in size depending on their size. The round mitochondrion is 0.2 microns to 2 microns in diameter. Mitochondrial mitochondria are 40 microns to 70 microns in length. Rod-shaped mitochondria can be 9 microns in length and 0.5 microns in width. The number of mitochondria varies from cell to cell. Mitochondrions are absent in bacteria and blue-green algae. Some algae have only 1 mitochondrion per cell. Normally there are 200 to 400 mitochondria per plant cell. Animal liver cells contain thousands of mitochondria. Fourteen thousand to millions of mitochondria have been observed in searching eggs.

Mitochondria play a crucial role in cell signaling and influence various cellular functions. Their potential involvement in cancer, especially in promoting tumor plasticity and advanced disease traits such as metastasis, has garnered significant interest. The microenvironment of tumor growth is highly detrimental to mitochondria, as erratic oxygen concentrations, low nutrients, and high oxidative radicals compromise their functionality.

In cancer, mitochondrial fitness is commonly lost, resulting in the formation of defective "ghost" mitochondria that relay signals of metabolic starvation, oxidative stress, and inflammation. Although mitochondria are important drivers of cancer, the mechanisms underlying this phenomenon are not yet fully understood. The prevailing view is that cancer exploits damaged and dysfunctional "ghost" mitochondria generated by the hostile tumor environment, rather than normal mitochondria from oxygenated and nutrient-replete tissues.

These "ghost" mitochondria, which evade quality control and prevent cell death, send multiple danger signals indicating metabolic starvation, cellular stress, and reprogrammed gene expression. Consequently, tumor cells acquire a new cellular phenotype that is quiescent in terms of proliferation but highly motile, enabling them to escape from unfavorable conditions and colonize distant, more favorable sites.

Conclusion:

It seems that early developmental outcomes depend on both mitochondria and mtDNA. Although it is unlikely that oocyte mitochondria contribute a significant amount of energy, their role as mtDNA carriers ensures that there is a sufficient amount of mtDNA copy. By producing effective electron transport chains and maintaining effective mitochondrial membrane potentials, sufficient mtDNA copy number likely promotes mitochondrial function and ensures that the mitochondria can mediate important functions that are not just limited to energy production.