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.
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 ...Show More
