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Article

SIRT1 suppresses pituitary tumor progression by downregulating PTTG1 expression

  • Authors:
    • Jinxiang Huang
    • Fenglin Zhang
    • Guohan Hu
    • Yuan Pan
    • Wei Sun
    • Lei Jiang
    • Peng Wang
    • Jiting Qiu
    • Xuehua Ding
  • View Affiliations / Copyright

    Affiliations: Department of Neurosurgery, Shanghai Institute of Neurosurgery, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai 200003, P.R. China, Department of Neurosurgery, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, P.R. China, Department of Neurosurgery, No. 971 Hospital of People's Liberation Army Navy, Qingdao, Shandong 266071, P.R. China, Department of Radiology, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai 200003, P.R. China, Department of Neurosurgery, Ruijin Hospital North, Shanghai Jiaotong University School of Medicine, Shanghai 201803, P.R. China
  • Article Number: 143
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    Published online on: June 21, 2022
       https://doi.org/10.3892/or.2022.8354
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Abstract

Although pituitary tumors are among the most common types of brain tumor, the underlying molecular mechanism of this disease remains obscure. To this end, the role of sirtuin 1 (SIRT1) in pituitary tumors was reported. The results of reverse transcription‑quantitative PCR and immunohistochemistry revealed that sirtuin 1 (SIRT1) expression was downregulated in the tumor tissues of patients with pituitary tumors. In vitro experiments of the present study demonstrated that SIRT1 upregulation suppressed pituitary tumor cell line growth, while SIRT1 downregulation demonstrated the opposite effect. Additionally, it was determined that the enzymatic activity of SIRT1 was required for its cellular function. A mechanistic experiment determined that SIRT1 negatively regulated pituitary tumor‑transforming gene 1 (PTTG1) expression through the deacetylation of histone (H)3 lysine (K)9ac at the promoter region of PTTG1. Moreover, H3K9ac levels at the PTTG1 promoter were determined to be an essential regulatory element for PTTG1 expression. Thus, it was concluded that the SIRT1/H3K9ac/PTTG1 axis contributed to pituitary tumor formation and may represent a potential therapeutic strategy.
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Copy and paste a formatted citation
Spandidos Publications style
Huang J, Zhang F, Hu G, Pan Y, Sun W, Jiang L, Wang P, Qiu J and Ding X: SIRT1 suppresses pituitary tumor progression by downregulating PTTG1 expression. Oncol Rep 48: 143, 2022.
APA
Huang, J., Zhang, F., Hu, G., Pan, Y., Sun, W., Jiang, L. ... Ding, X. (2022). SIRT1 suppresses pituitary tumor progression by downregulating PTTG1 expression. Oncology Reports, 48, 143. https://doi.org/10.3892/or.2022.8354
MLA
Huang, J., Zhang, F., Hu, G., Pan, Y., Sun, W., Jiang, L., Wang, P., Qiu, J., Ding, X."SIRT1 suppresses pituitary tumor progression by downregulating PTTG1 expression". Oncology Reports 48.2 (2022): 143.
Chicago
Huang, J., Zhang, F., Hu, G., Pan, Y., Sun, W., Jiang, L., Wang, P., Qiu, J., Ding, X."SIRT1 suppresses pituitary tumor progression by downregulating PTTG1 expression". Oncology Reports 48, no. 2 (2022): 143. https://doi.org/10.3892/or.2022.8354
Copy and paste a formatted citation
x
Spandidos Publications style
Huang J, Zhang F, Hu G, Pan Y, Sun W, Jiang L, Wang P, Qiu J and Ding X: SIRT1 suppresses pituitary tumor progression by downregulating PTTG1 expression. Oncol Rep 48: 143, 2022.
APA
Huang, J., Zhang, F., Hu, G., Pan, Y., Sun, W., Jiang, L. ... Ding, X. (2022). SIRT1 suppresses pituitary tumor progression by downregulating PTTG1 expression. Oncology Reports, 48, 143. https://doi.org/10.3892/or.2022.8354
MLA
Huang, J., Zhang, F., Hu, G., Pan, Y., Sun, W., Jiang, L., Wang, P., Qiu, J., Ding, X."SIRT1 suppresses pituitary tumor progression by downregulating PTTG1 expression". Oncology Reports 48.2 (2022): 143.
Chicago
Huang, J., Zhang, F., Hu, G., Pan, Y., Sun, W., Jiang, L., Wang, P., Qiu, J., Ding, X."SIRT1 suppresses pituitary tumor progression by downregulating PTTG1 expression". Oncology Reports 48, no. 2 (2022): 143. https://doi.org/10.3892/or.2022.8354
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