TRIM52 knockdown inhibits cell proliferation and induces apoptosis through activation of the STAT3 pathway in ovarian cancer¹

Abstract

Ovarian cancer (OC) is a common gynecologic malignancy worldwide. Several members of the tripartite motif (TRIM) family are of great importance in various human malignancies. In this study, we aimed to figure out the function and mechanism of TRIM52 in OC. Western blot and RT–PCR were used to examine the expression level of TRIM52. Cell counting kit-8 (CCK-8) assay was used to measure cell proliferation. Annexin V/ PI kit and TUNEL assay were carried out to test cell apoptosis. Knockdown of TRIM52 significantly inhibited cell proliferation and induced cell apoptosis. Glucose uptake, lactate, and ATP production were depressed after TRIM52 silencing. Furthermore, loss of TRIM52 decreased the levels of pyruvate kinase isozyme M2, glucose transporter protein 1, and p-STAT3. Overexpression of TRIM52 showed effects that were opposite as those of TRIM52 knockdown; these effects were alleviated by AG490, which is an inhibitor of STAT3. In addition, TRIM52 knockdown inhibited tumorigenesis in a xenograft mouse model. Finally, we found that high level of TRIM52 expression predicted poor prognosis. In conclusion, TRIM52 knockdown inhibited cell proliferation and induced apoptosis through the activation of STAT3 signaling.

KEYWORDS:

• Ovarian cancer
• TRIM52
• STAT3

Data availability statement

The data that support the findings of this study are available in ‘figshare’ [https://figshare.com/] at

http://doi.org/10.6084/m9.figshare.14702145

http://doi.org/10.6084/m9.figshare.14702148

http://doi.org/10.6084/m9.figshare.14702160

http://doi.org/10.6084/m9.figshare.14702169

http://doi.org/10.6084/m9.figshare.14702175

http://doi.org/10.6084/m9.figshare.14702181

http://doi.org/10.6084/m9.figshare.14702184

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This work was supported by the Natural Science Foundation of the Tibet Autonomous Region [grant number XZ2017ZRG-78(Z)].