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SUN Man, YANG Xiao-wen, CAO Feng, et al. Downregulation of SND1 Expression Accelerates Cell Senescence of Human Diploid Fibroblasts 2BS via Modulating the SASP[J]. Journal of Sichuan University (Medical Sciences), 2020, 51(3): 365-370. DOI: 10.12182/20200560504
Citation: SUN Man, YANG Xiao-wen, CAO Feng, et al. Downregulation of SND1 Expression Accelerates Cell Senescence of Human Diploid Fibroblasts 2BS via Modulating the SASP[J]. Journal of Sichuan University (Medical Sciences), 2020, 51(3): 365-370. DOI: 10.12182/20200560504

Downregulation of SND1 Expression Accelerates Cell Senescence of Human Diploid Fibroblasts 2BS via Modulating the SASP

  •   Objective  To investigate the effect of down-regulation of SND1 expression on senescence of human diploid fibroblasts.
      Methods  Western blot and immunohistochemistry were used to detect the expression of SND1 in young or senescent 2BS cells and aged tissues. Immunofluorescence was conducted to detect the localization of SND1 in young 2BS cells. CCK8 and EDU were performed to detect the proliferation of 2BS. Colony formation analysis was used to evaluate the capacity of colony formation of 2BS. Expression chip and RT-qPCR analysis were performed to detect the change of SASP expression level. β-galactosidase staining was employed to indicate the senescent 2BS cells.
      Results  The expression of SND1 in the senescent 2BS cells was significantly down-regulated compared with in the younger 2BS cells, and in human colon adenomas, its expression was also significantly down-regulated compared with in non-lesion colon tissues. In young 2BS, knockdown of SND1 inhibited the proliferation and colony formation of 2BS, and led to stronger senescence-associated beta-galactosidase staining (SA-β-gal). Expression chip and RT-qPCR analysis indicated that knockdown of SND1 up-regulated the expression of senescence-associated secretory phenotype components (SASP).
      Conclusions  Our data indicated that down-regulation of SND1 regulated human diploid cell senescence by up-regulating the expression of SASP components.
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