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. 2019 Jun 24;11:5725–5735. doi: 10.2147/CMAR.S210782

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© 2019 Shen et al.

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).

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TRIM14 regulated the PTEN/AKT signaling pathway. (A, B) Protein levels of PTEN, p-AKT, AKT, Bcl-2, Cyclin D1, and p27 were determined in the indicated colorectal cancer (CRC) cells at 48 hrs after viral infection. (C, D) mRNA expression of PTEN, Bcl-2, Cyclin D1, and p27 was assessed in the indicated CRC cells at 48 hrs after viral infection. shNC or pLVX served as negative control. ***P<0.001 vs shNC or pLVX. (E) LoVo cells were fixed and stained with TRIM14 (green) and PTEN (red) antibodies. Nuclei were stained with DAPI (blue). Representative images are shown. Scale bar: 20 μm. (F) Effects of TRIM14 on PTEN ubiquitination.

Abbreviation: shNC, lentiviral plasmid expressing control short hairpin RNA.