Immune Netw.  2002 Dec;2(4):183-188. 10.4110/in.2002.2.4.183.

Telomerase: Key to Mortal or Immortal Road

Affiliations
  • 1Samsung Biomedical Research Institute, Molecular Therapy Research Center, Samsung Medical Center, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, Korea. hwl@skku.ac.kr

Abstract

Gradual attrition of telomere to a critical short length elicits successive cellular response of cellular senescence and crisis. Cancer cells evade this process by maintaining functional telomeres via one of two known mechanisms of telomere maintenance. The first and most frequent mechanism involves reactivation of enzyme activity of telomerase, a ribonucleoprotein complex mainly via transcriptional up-regulation of TERT, a catalytic subunit of telomerase complex. The second mechanism utilizes telomerase-independent way termed ALT (for Alternative Lengthening of Telomere), which possibly involves recombination pathways. Thus master key for cellular immortalization is supposed to possess adequate telomere reserves. Indeed, telomerase can alone induce the immortalization under culture on feeder cell layers without generally known inactivation mechanism of tumor suppressor genes. Including this phenomena, this review will focus on telomerase and telomere-associated proteins, thereby implication of these proteins for cellular immortalization processes.

Keyword

Telomere; telomerase; telomere-binding protein; immortalization; tumorigenesis

MeSH Terms

Carcinogenesis
Catalytic Domain
Cell Aging
Feeder Cells
Genes, Tumor Suppressor
Recombination, Genetic
Ribonucleoproteins
Telomerase*
Telomere
Up-Regulation
Ribonucleoproteins
Telomerase
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