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Full Version: Interlink Between Telomeres and Cancer
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Cancer has always been a very intriguing subject of research as no permanent cure has been developed for it yet. Different factors responsible for causing cancer like the presence of many genes, proteins, etc in the tumor cells have been identified but still no vaccine or medicine has been discovered for curing cancer completely and permanently due to the rapid rate of proliferation of the tumor cells and their unpredictable nature of localization and differentiation. Moreover, the different treatments as chemotherapy, radiation, etc seem to affect the nearby normal cells drastically as the targeting of tumor cells specifically is very difficult. Every day a new research regarding it is developed and a new factor responsible for cancer development is found, making the research study on cancer a never-ending subject.

The Cell Cycle is studied to a great extent during cancer research. DNA undergoes replication and in this process, the end replication problem, which causes loss of important sequences of genes present at the ends of the DNA. Thousands of tandem repeats of hexa-nucleotide sequence TTAGGG are present in the repetitive non-coding DNA along with proteins. They are known as telomeres. The cell phenotype of the cells is controlled by the presence of telomeres, though the exact relationship between them is quite complex. The telomeres play an important role in tumorigenesis, cell cycle regulation, genomic stability, etc. The telomeres are present in the ends of the chromosomes and help in the recognition of the actual ends of linear double-stranded DNA from the breaks within the double-stranded DNA. The telomere undergoes shortening with each cycle of replication and the ultimate Cell senescence or growth arrest is determined by the maximum number of replication cycles undergone by the DNA to reach the optimal length of the telomeres. Actually, the telomeres possess a cap like structure made of different proteins and these proteins are responsible for DNA strand repair and regulation of telomere length.

The tumor suppressor proteins p53 and Rb are present within the cell and are known as downstream effectors. They regulate cell proliferation, as they are responsible for the senescence or permanent arrest in growth of the cell, which is imposed on the cell once the telomeric DNA reaches the optimum length. The telomere shortening process triggers the activation of the pathways involving the production of the p53 and Rb proteins, thereby activating the process of cell senescence. The suppression of the genes encoding these proteins resulted in the development of immortal cells, due to suppression of cell senescence.

Some cells bypass senescence or cell growth arrest by the inactivation of the signalling pathways of p53 and Rb. These cells undergo cell division until the telomere length is shortened critically. This causes the end-to-end fusion of the DNA and the trigger of DNA- strand break repair mechanisms. Hence, these cells devise mechanisms, in which they maintain the telomere length by alternative pathways (ALT). In this pathway, the telomerase, which is a reverse transcriptase enzyme, plays an important role in using associated RNA to increase the length of the telomeric ends, which has been demonstrated by the cloning of the hTERT (human Telomerase Reverse Transcriptase) encoding gene. The role of telomerase in cellular immortality was shown in different cells like retinal pigment epithelial cells, fibroblasts, endothelial cells, etc.

The normal cells undergo a number of mutations, which result in a number of transformations. These transformations give rise to a number of changes in the cellular functions and properties like the uncontrolled division of cells resulting in the immortality of the cells and thus formation of tumor cells. Apart from the suppression of cell senescence, the loss of integrity of the telomeres is also an important factor resulting in the formation and development of tumor cells. The uncontrolled division of cells result in very short telomeres that ultimately cause fusion in the ends of DNA resulting in genomic instability and thus the transformation of cells. The telomere length is maintained in 90% of transformed, tumor cells by the expression of the hTERT gene. Hence, it is seen that the telomeres and their related proteins play a very important role in tumorigenesis, leading ultimately to cancer and that telomeric integrity and homeostasis are very vital for the maintenance of genomic stability within the cell.
I was doing some technology analysis on Telomere. Some resources say that if you improve the depend of telomere it can opposite aging but, also cause cancer. Can anyone describe how it cause cancer, Any ideas?

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