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Updated: Feb 16, 2026
Generation of Cancer Cell Clones to Visualize Telomeric Repeat-containing RNA TERRA Expressed from a Single Telomere in Living Cells
Published on: January 17, 2019
Telomeres in cancer
Cagatay Gunes1, Alush Irene Avila2, K Lenhard Rudolph2
1Department of Urology, Ulm University, Germany.
Abstract:
Telomere shortening as a consequence of cell divisions during aging and chronic diseases associates with an increased cancer risk. Experimental data revealed that telomere shortening results in telomere dysfunction, which in turn affects tumorigenesis in two ways. First, telomere dysfunction suppresses tumor progression by the activation of DNA damage checkpoints, which induce cell cycle arrest (senescence) or apoptosis, as well as by inducing metabolic compromise and activation of immune responses directed against senescent cells. Second, telomere dysfunction promotes tumorigenesis by inducing chromosomal instability in tumor initiating cells, by inhibiting proliferative competition of non-transformed cells, and possibly, also by influencing tumor cell plasticity. The tumor promoting effects of telomere dysfunction are context dependent and require the loss of p53-dependent DNA damage checkpoints or other genetic modifiers that attenuate DNA damage responses possibly involving complex interactions of different genes. The activation of telomere stabilizing mechanisms appears as a subsequent step, which is required to enable immortal grotwh of emerging cancer cells. Here, we conceptually discuss our current knowledge and new, unpublished experimental data on telomere dependent influences on tumor initiation and progression.
Insights
Telomere shortening, linked to aging and disease, can both suppress and promote cancer. Telomere dysfunction
Area of Science:
- Oncology
- Cell Biology
- Genetics
Background:
- Telomere shortening occurs with aging and chronic diseases, increasing cancer risk.
- Telomere dysfunction has dual roles in tumorigenesis, suppressing or promoting tumor development.
Purpose of the Study:
- To discuss current knowledge and new data on telomere-dependent influences on tumor initiation and progression.
- To explore the dual role of telomere dysfunction in cancer development.
Main Methods:
- Conceptual discussion of experimental data.
- Analysis of telomere dysfunction's impact on DNA damage checkpoints, senescence, apoptosis, and immune responses.
- Examination of telomere dysfunction's role in chromosomal instability and tumor cell plasticity.
Main Results:
- Telomere dysfunction can suppress tumors via DNA damage checkpoints, senescence, apoptosis, metabolic compromise, and immune activation.
- Telomere dysfunction can promote tumors by inducing chromosomal instability and altering cellular competition and plasticity.
- Tumor promotion by telomere dysfunction is context-dependent, often requiring loss of p53 or other genetic modifiers.
Conclusions:
- Telomere dysfunction presents a complex, context-dependent role in cancer initiation and progression.
- Telomere stabilization is a critical step for cancer cell immortalization.
- Understanding telomere dynamics is crucial for cancer research and therapeutic strategies.
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