Telomere and telomerase function: safeguarding chromosomal ends and their implications in aging and cancer development

Abstract

Introduction. Telomeres, the protective caps at the ends of linear chromosomes, play a crucial role in maintaining genomic stability and integrity. As cells undergo repeated divisions, telomeres progressively shorten, eventually leading to cellular senescence or apoptosis. Aim of study. The fundamental aspects of telomere function, its significance in safeguarding chromosomal ends, and the implications of telomere dynamics in the processes of aging and cancer development. Methods and materials: 26 articles from PubMed and ScienceDirect. The keywords employed in this analysis included "telomeres," "aging," and "cancer". Results: Telomeres present at the ends of the q and p arms of chromosomes consist of repetitive TTAGGG sequences. Their function is to prevent the fusion of non-homologous chromatids, chromosomal degradation, recombination and protecting genetic information. Telomere length becomes a "biomarker" in the aging process and the onset of various diseases, such as cancer development. The aging process leads to telomere shortening, and chromosomes lose their capabilities and stability. This results in numerous chromosomal rearrangements that can lead to apoptosis or replicative senescence. The telomere shortening process is dependent on the replication direction of linear molecules guided by DNA polymerase. DNA synthesis initiation requires an RNA primer, leading to DNA losses with each somatic cell division, causing telomeres to decrease in size. The gradual reduction in telomere length during replication cycles is associated with the activation of pRB and p53 pathways to genomic instability and replicative senescence. Telomerase, a ribonucleoprotein enzyme, counteracts telomere shortening by adding repetitive DNA sequences to chromosomal ends. Telomerase activity is regulated, with implications in both aging and cancer. Investigations into telomerase regulation and telomere length include cloning RNA components, telomerase-associated proteins, and antisense experiments demonstrating progressive telomere shortening in the absence of telomerase. Additionally, the identification of telomere-binding proteins suggests a regulatory role through negative feedback signals. Therapeutic regulation of telomerase activity holds promise in cancer therapy, as telomere shortening and maintenance are identified as crucial events in tumor formation. Cancer cells often achieve immortality through telomerase activation or alternative lengthening of telomeres mechanisms, allowing uncontrolled proliferation. Conclusion. The role of telomeres and the telomerase offers the possibility to slow down the aging process, preserve cellular immunity, and to prevent tumors, thus opening up potential therapeutic directions. Continuous research in this field is necessary to unlock the full potential of these molecular entities in shaping the cellular life trajectory and preservation. role in maintaining genomic stability and integrity. As ce lls undergo repeated divisions, telomeres progressively shorten, eventually leading to cellular sene scence or apoptosis. Aim of study. The fundamental aspects of telomere function, its sig nificance in safeguarding chromosomal ends, and the implications of telomere dyn amics in the processes of aging and cancer development. Methods and materials: 26 articles from PubMed and ScienceDirect. The keywords em ployed in this analysis included "telomeres," "aging," and "cancer". Results: Telomeres present at the ends of the q and p arms of chr omosomes consist of repetitive TTAGGG sequences. Their function is to prevent the fusio n of non-homologous chromatids, chromosomal degradation, recombination and protecting genetic information. Telomere length becomes a "biomarker" in the aging process and the onset of various diseases, such as cancer development. The aging process leads to telomere shortenin g, and chromosomes lose their capabilities and stability. This results in numerous chromo somal rearrangements that can lead to apoptosis or replicative senescence. The telomere shor tening process is dependent on the replication direction of linear molecules guided by DNA polymerase. DNA synthesis initiation requires an RNA primer, leading to DNA losses with each s omatic cell division, causing telomeres to decrease in size. The gradual reduction in telomere lengt h during replication cycles is associated with the activation of pRB and p53 pathways to genomic inst ability and replicative senescence. Telomerase, a ribonucleoprotein enzyme, counteracts telo mere shortening by adding repetitive DNA sequences to chromosomal ends. Telomerase activity is regulated, with implications in both aging and cancer. Investigations into telomerase regulat ion and telomere length include cloning RNA components, telomerase-associated proteins, and antis ense experiments demonstrating progressive telomere shortening in the absence of telom erase. Additionally, the identification of telomere-binding proteins suggests a regulatory role through negative feedback signals. Therapeutic regulation of telomerase activity holds promis e in cancer therapy, as telomere shortening and maintenance are identified as crucial even ts in tumor formation. Cancer cells often achieve immortality through telomerase activation or alt ernative lengthening of telomeres mechanisms, allowing uncontrolled proliferation. Conclusion. The role of telomeres and the telomerase offers the possibility to slow down the aging process, preserve cellular immunity, and to prevent tumors, t hus opening up potential therapeutic directions. Continuous research in this field is necessa ry to unlock the full potential of these molecular entities in shaping the cellular life trajector y and preservation.