TRIM58 Interacts with Pyruvate Kinase M2 to Inhibit Tumorigenicity in Human Osteosarcoma Cells

TRIM58 与丙酮酸激酶 M2 相互作用抑制人类骨肉瘤细胞的致瘤性

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作者:Peng Yuan, Yiyi Zhou, Rui Wang, Shayang Chen, Qiqi Wang, Zhujie Xu, Yi Liu, Huilin Yang

Background

Tripartite motif containing 58 (TRIM58), an E3 ubiquitin ligase, is reported as a suppressor gene in certain human tumors. However, the biological function of TRIM58 in osteosarcoma (OS) is still less identified.

Conclusions

This analysis not only explored a deep understanding of the biological function of TRIM58 but also indicated its signaling pathway in OS cells.

Methods

In the present study, TRIM58 induced silencing and overexpression in OS cells using RNA interference (RNAi) and lentiviral-mediated vector, respectively. Cell proliferation profiles were analyzed using cell counting kit-8 (CCK-8) assay. Cell apoptosis profiles were determined using a flow cytometer. qRT-PCR and western blot were used to determine gene expression. Coimmunoprecipitation (Co-IP) assay was used to examine protein interaction.

Results

Our results demonstrated TRIM58 was downregulated in human OS tissues. Overexpression of TRIM58 remarkably suppressed the growth of OS cells and decreased glucose transportation and lactate secretion. These results indicated that TRIM58 involved in the regulation of energy metabolism in OS cells. Importantly, TRIM58 interacted with pyruvate kinase M2 (PKM2) in OS cells. Moreover, TRIM58 might inhibit the activity of PKM2 through enhancing its polyubiquitination in OS cells. Conclusions: This analysis not only explored a deep understanding of the biological function of TRIM58 but also indicated its signaling pathway in OS cells.

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