TRIM28 promotes cervical cancer growth through the mTOR signaling pathway

  • Authors:
    • Fan Li
    • Zhijie Wang
    • Gaochuan Lu
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  • Published online on: January 26, 2018     https://doi.org/10.3892/or.2018.6235
  • Pages: 1860-1866
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Abstract

Aberrant expression of tripartite motif-containing protein 28 (TRIM28) has been demonstrated in several human cancers; however, its biological function and related mechanism in cervical cancer remain unclear. In this study, we compared TRIM28 expression between cervical cancer and adjacent normal tissues, and detected significant elevation in TRIM28 expression levels in the cervical cancer tissues. Moreover, TRIM28 overexpression promoted the proliferation, colony formation, and cell cycle progression of cervical cancer cell lines, as well as the growth of xenograft tumors in nude mice, whereas knockdown of TRIM28 had the opposite effects. Evaluation of the potential mechanism demonstrated that TRIM28 promoted cervical cancer cell growth by activating the mammalian target of rapamycin (mTOR) signaling pathway. In support of this finding, TRIM28-induced cell proliferation was abolished by treatment with everolimus, a specific mTOR inhibitor. These results suggest that TRIM28 plays a pivotal role in cervical cancer cell proliferation and might serve as a potential therapeutic target.
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April-2018
Volume 39 Issue 4

Print ISSN: 1021-335X
Online ISSN:1791-2431

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Copy and paste a formatted citation
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Spandidos Publications style
Li F, Wang Z and Lu G: TRIM28 promotes cervical cancer growth through the mTOR signaling pathway. Oncol Rep 39: 1860-1866, 2018.
APA
Li, F., Wang, Z., & Lu, G. (2018). TRIM28 promotes cervical cancer growth through the mTOR signaling pathway. Oncology Reports, 39, 1860-1866. https://doi.org/10.3892/or.2018.6235
MLA
Li, F., Wang, Z., Lu, G."TRIM28 promotes cervical cancer growth through the mTOR signaling pathway". Oncology Reports 39.4 (2018): 1860-1866.
Chicago
Li, F., Wang, Z., Lu, G."TRIM28 promotes cervical cancer growth through the mTOR signaling pathway". Oncology Reports 39, no. 4 (2018): 1860-1866. https://doi.org/10.3892/or.2018.6235