Glioblastoma (GBM) is a kind of intractable brain tumor. The effect of surgical treatment, radiotherapy and chemotherapy is not ideal. TRF1 is one of the important components of shelterin complex, which plays an important role in human telomere protection. Previous studies have reported that inhibition of TRF1 expression can inhibit the growth and proliferation of GBM without causing serious physiological dysfunction. However, the specific mechanism of inhibition of GBM growth and proliferation caused by decreased TRF1 expression has not been fully elucidated. To further elucidate this mechanism, we knockdown TRF1 by siRNA. We detected the levels of cell senescence, autophagy through biological experiments. It has been found that the knockdown of TRF1 can cause significant increase in the aging, autophagy of GBM. In addition, SIRT-6 is a NAD+- dependent deacetylase. Previous studies have reported that SIRT-6 can maintain the stability of telomere function. Moreover, telomere dysfunction can cause the decrease of SIRT-6 expression. Therefore, we want to study the effect of SIRT-6 expression level on TRF1 knockdown induced aging, autophagy in GBM. The experimental results showed that the knockdown of TRF1 caused the decrease of SIRT-6 expression level, and the increase of SIRT-6 expression level could inhibit the aging, autophagy caused by TRF1 knockdown. This study provides a new direction for the treatment of GBM.
| Published in | International Journal of Biomedical Engineering and Clinical Science (Volume 11, Issue 2) |
| DOI | 10.11648/j.ijbecs.20251102.11 |
| Page(s) | 11-27 |
| Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
| Copyright |
Copyright © The Author(s), 2025. Published by Science Publishing Group |
Glioblastoma, TRF1, SIRT-6, Autophagy, Senescence, Telomere Damage
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APA Style
Nie, Z., Liu, S., Huang, X., Geng, X. (2025). Inhibition of TRF1 Can Accelerate Aging and Induce Autophagy Through the P53-SIRT6 Pathway in Glioblastoma Multiforme. International Journal of Biomedical Engineering and Clinical Science, 11(2), 11-27. https://doi.org/10.11648/j.ijbecs.20251102.11
ACS Style
Nie, Z.; Liu, S.; Huang, X.; Geng, X. Inhibition of TRF1 Can Accelerate Aging and Induce Autophagy Through the P53-SIRT6 Pathway in Glioblastoma Multiforme. Int. J. Biomed. Eng. Clin. Sci. 2025, 11(2), 11-27. doi: 10.11648/j.ijbecs.20251102.11
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Download@article{10.11648/j.ijbecs.20251102.11,
author = {Ziyang Nie and Siqi Liu and Xinyu Huang and Xin Geng},
title = {Inhibition of TRF1 Can Accelerate Aging and Induce Autophagy Through the P53-SIRT6 Pathway in Glioblastoma Multiforme
},
journal = {International Journal of Biomedical Engineering and Clinical Science},
volume = {11},
number = {2},
pages = {11-27},
doi = {10.11648/j.ijbecs.20251102.11},
url = {https://doi.org/10.11648/j.ijbecs.20251102.11},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ijbecs.20251102.11},
abstract = {Glioblastoma (GBM) is a kind of intractable brain tumor. The effect of surgical treatment, radiotherapy and chemotherapy is not ideal. TRF1 is one of the important components of shelterin complex, which plays an important role in human telomere protection. Previous studies have reported that inhibition of TRF1 expression can inhibit the growth and proliferation of GBM without causing serious physiological dysfunction. However, the specific mechanism of inhibition of GBM growth and proliferation caused by decreased TRF1 expression has not been fully elucidated. To further elucidate this mechanism, we knockdown TRF1 by siRNA. We detected the levels of cell senescence, autophagy through biological experiments. It has been found that the knockdown of TRF1 can cause significant increase in the aging, autophagy of GBM. In addition, SIRT-6 is a NAD+- dependent deacetylase. Previous studies have reported that SIRT-6 can maintain the stability of telomere function. Moreover, telomere dysfunction can cause the decrease of SIRT-6 expression. Therefore, we want to study the effect of SIRT-6 expression level on TRF1 knockdown induced aging, autophagy in GBM. The experimental results showed that the knockdown of TRF1 caused the decrease of SIRT-6 expression level, and the increase of SIRT-6 expression level could inhibit the aging, autophagy caused by TRF1 knockdown. This study provides a new direction for the treatment of GBM.
},
year = {2025}
}
TY - JOUR T1 - Inhibition of TRF1 Can Accelerate Aging and Induce Autophagy Through the P53-SIRT6 Pathway in Glioblastoma Multiforme AU - Ziyang Nie AU - Siqi Liu AU - Xinyu Huang AU - Xin Geng Y1 - 2025/05/29 PY - 2025 N1 - https://doi.org/10.11648/j.ijbecs.20251102.11 DO - 10.11648/j.ijbecs.20251102.11 T2 - International Journal of Biomedical Engineering and Clinical Science JF - International Journal of Biomedical Engineering and Clinical Science JO - International Journal of Biomedical Engineering and Clinical Science SP - 11 EP - 27 PB - Science Publishing Group SN - 2472-1301 UR - https://doi.org/10.11648/j.ijbecs.20251102.11 AB - Glioblastoma (GBM) is a kind of intractable brain tumor. The effect of surgical treatment, radiotherapy and chemotherapy is not ideal. TRF1 is one of the important components of shelterin complex, which plays an important role in human telomere protection. Previous studies have reported that inhibition of TRF1 expression can inhibit the growth and proliferation of GBM without causing serious physiological dysfunction. However, the specific mechanism of inhibition of GBM growth and proliferation caused by decreased TRF1 expression has not been fully elucidated. To further elucidate this mechanism, we knockdown TRF1 by siRNA. We detected the levels of cell senescence, autophagy through biological experiments. It has been found that the knockdown of TRF1 can cause significant increase in the aging, autophagy of GBM. In addition, SIRT-6 is a NAD+- dependent deacetylase. Previous studies have reported that SIRT-6 can maintain the stability of telomere function. Moreover, telomere dysfunction can cause the decrease of SIRT-6 expression. Therefore, we want to study the effect of SIRT-6 expression level on TRF1 knockdown induced aging, autophagy in GBM. The experimental results showed that the knockdown of TRF1 caused the decrease of SIRT-6 expression level, and the increase of SIRT-6 expression level could inhibit the aging, autophagy caused by TRF1 knockdown. This study provides a new direction for the treatment of GBM. VL - 11 IS - 2 ER -
Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, ChinaKey Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Medical University, Tianjin, China Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Medical University, Tianjin, China School of Life Sciences, Central China Normal University, Wuhan, China
Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Medical University, Tianjin, China
Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Medical University, Tianjin, China
Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Medical University, Tianjin, China
