Volume 42 Issue 8
Aug.  2021
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Jian-wei SUN, Qian XIANG, Zi-chao LIU, Shan-shan XU, Ding DING. Effect of PTEN Gene Expression on Apoptosis of Thyroid Cancer Cells BCPAP and FTC133 and Expression of ERK and AKT[J]. Journal of Kunming Medical University, 2021, 42(8): 23-30. doi: 10.12259/j.issn.2095-610X.S20210805
Citation: Jian-wei SUN, Qian XIANG, Zi-chao LIU, Shan-shan XU, Ding DING. Effect of PTEN Gene Expression on Apoptosis of Thyroid Cancer Cells BCPAP and FTC133 and Expression of ERK and AKT[J]. Journal of Kunming Medical University, 2021, 42(8): 23-30. doi: 10.12259/j.issn.2095-610X.S20210805

Effect of PTEN Gene Expression on Apoptosis of Thyroid Cancer Cells BCPAP and FTC133 and Expression of ERK and AKT

doi: 10.12259/j.issn.2095-610X.S20210805
  • Received Date: 2021-06-15
    Available Online: 2021-08-04
  • Publish Date: 2021-08-04
  •   Objective  To investigate the effect of PTEN gene expression on the apoptosis of BCPAP cells and FTC133 thyroid cancer cells and on the expression of signal pathway proteins ERK and AKT.  Methods  BCPAP cells and FTC133 cells were transfected with PTEN-pCMV6 and silenced si-PTEN RNA, before the cell microscopic morphology changes were observed. Cell viability was measured by MTT, and apoptosis rate was measured by Annexin V-FITC and PI double staining flow cytometer, respectively. Furthermore, the protein expression levels of ERK, AKT, Bax, Bcl-2, caspase 8, 9, 12 and 3 were detected by Western blot. The association between different expression of PTEN gene and the apoptosis of BCPAP and FTC133 thyroid cancer cells and the expression of signal pathway proteins were analyzed.  Results  Compared with control group, when the PTEN gene was overexpressed, BCPAP and FTC133 thyroid cancer cells showed microscopic apoptotic changes such as deformation, volume reduction and nuclear pyknosis. The cell viability was decreased (P < 0.01), and the cell apoptosis rate was increased (P < 0.01). The expression levels of the apoptotic proteins caspase 8, 9, 12, 3, and proapoptotic protein Bax were significantly increased (P < 0.01), and the expression of anti-apoptotic protein Bcl-2 was significantly decreased (P < 0.01), the expression of ERK and AKT were decreased (P < 0.05). The reduction degree of ERK relative expression in FTC133 cells was significantly higher than that in BCPAP cells (P < 0.01), while the reduction degree of AKT relative expression in BCPAP and FTC133 cells was not statistically significant (P > 0.05). After PTEN gene silencing, compared with the control group, the number, cell morphology, volume and nuclear morphology of BCPAP and FTC133 were not significantly different (P > 0.05). The change of cell viability and apoptosis rate were not significantly different (P > 0.05). The expression levels of apoptotic proteins caspase 8, 9, 12, 3, and proapoptotic protein Bax was significantly decreased (P < 0.01), and the expression level of anti-apoptotic protein Bcl-2 were significantly increased (P < 0.01). The expression levels of ERK and AKT in FTC133 cells were higher than those in the control group (P < 0.01), and the expression levels of ERK in BCPAP cells were higher than those in the control group (P < 0.01). Compared with the control group, there was no statistically significant difference in the expression level of AKT (P > 0.05). The relative expression level of ERK increased in BCPAP and FTC133, but there was no statistically significant difference (P > 0.05). The relative expression level of AKT increased in FTC133 cells than that in BCPAP cells (P < 0.05).  Conclusion  PTEN gene promotes the apoptosis of BCPAP and FTC133 cells. Mitochondrial pathway, death receptor pathway and endoplasmic reticulum activation pathway are all involved in the process of BCPAP and FTC133 cell apoptosis. ERK plays an important role in PTEN gene regulation of BCPAP cell apoptosis, while AKT and ERK both are involved in the process of PTEN gene promoting FTC133 apoptosis.
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