Expression of the human TRIM14 and its mutant form (P207L) promotes apoptosis in transgenic loaches

Abstract

The tripartite-motif (TRIM)14 protein, one of the TRIM family members, was shown to participate in the antiviral and antibacterial defence. Besides, it appears to play an essential role in the processes of oncogenesis. In some types of human tumour cells, TRIM14 has been shown to inhibit apoptosis, while in others-the overexpression of TRIM14 promotes apoptosis. However, whether TRIM14 mediates apoptosis in the normal cells remains unknown. In the present study, we investigated the possible participation of the human TRIM14 gene and its mutant form (620C > T) in the induction of apoptosis in the transgenic larvae loach Misgurnus fossilis L. We observed that the expression of both forms of TRIM14 gene was accompanied by the increase of the frequency of pyknotic nuclei in fish embryos compared to control groups. Accordingly, using the TUNEL assay, the enhanced apoptosis was revealed upon expression of both forms of TRIM14 gene. The transcription of proapoptotic genes (bax, tp53, and casp9) was significantly increased in transgenic loaches expressing human wild-type TRIM14, but remained unchanged upon expression of its mutant form. In addition, the transcription of c-myc was upregulated in transgenic loaches expressing both forms. Thus, it can be assumed that during embryonic development TRIM14 has a proapoptotic effect on the cells via the activation of c-myc, tp53, and bax genes. Apparently, the mutant TRIM14 directs apoptosis via c-myc by p53-independent mechanism.

Expression profile of Tripartite motif family (TRIM) in human fibroblasts (NHDF) infected with porcine endogenous retrovirus (PERV)

“…In their work, Jia et al noted that to prevent excessive immune activation, mechanisms that suppress the TRIM14 expression, such as ring‐finger protein 125 (RNF125), are extremely important 31 . High levels of the TRIM14 expression were observed in connection with HIV and SIV infections 32 . In contrast to our results, a high expression level was also found in the case of influenza A, HCV, and rhinovirus infections 33‐35 .…”

Downregulation of miR-3568 Protects Against Ischemia/Reperfusion-Induced Cardiac Dysfunction in Rats and Apoptosis in H9C2 Cardiomyocytes Through Targeting TRIM62

“…It is exciting that these data were confirmed in H9C2 cardiomyocytes. The subcellular localization showed that TRIM protein family were located in cytosol and nucleus, and some TRIM proteins are capable to induce apoptosis, while the others, on the contrary, have an inhibitory effect on this process (Nenasheva and Stepanenko, 2018). TRIM69 regulated cell apoptosis through p53 signaling (Han et al, 2016).…”

TRIM family contribute to tumorigenesis, cancer development, and drug resistance

“…TRIM29 could bind to Tip60, and reduce acetylation of p53 at lysine 120 by Tip60, promoting cancer cell proliferation and enhancing transformation [ 165 ]. TRIM14 was reported to activate C-myc, p53, and Bax gene expression during embryonic development to modulate apoptosis [ 166 ]. TRIM32 [ 167 ].…”