Analysis of TRIM59 expression and its clinical significance in ovarian cancer by integrated bioinformatics

  • ZHENG Shunxin ,
  • ZHAO Maocheng ,
  • WEN Hongwei ,
  • JIANG Lifang
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  • Department of Clinical laboratory, Tanzhong People′s Hospital of Liuzhou, Liuzhou 545007, China

Received date: 2025-03-18

  Online published: 2025-12-17

Abstract

Objective: To explore the expression and clinical value of tripartite motif containing 59 (TRIM59) gene in ovarian cancer based on bioinformatics. Methods: The expression of TRIM59 mRNA in ovarian cancer tissues and ovarian tissues was analyzed by data sets in GEPIA database and GEO database. The expression of TRIM59 protein in ovarian cancer and ovarian tissue was analyzed in The Human Protein Atlas database. Kaplan-Meier database was used to study the correlation between TRIM59 expression and prognosis of ovarian cancer patients. Genes co-expressed with TRIM59 in ovarian cancer were screened from ULACAN database, and GO analysis and KEGG enrichment analysis were performed in DAVID database. The relationship between the expression of TRIM59 mRNA and the infiltration of various immune cells in ovarian cancer was analyzed in TIMER database. Results: The expression level of TRIM59 mRNA in ovarian cancer tissues was significantly higher than that in normal ovarian tissues, and this differential expression was closely related to the survival time of ovarian cancer patients. The results of immunohistochemistry showed that the positive rate of TRIM59 protein in ovarian cancer tissues was 75%, and no expression was found in normal ovarian tissues. In ovarian cancer tissues, 148 co-expressed genes were positively correlated with TRIM59, which were mainly involved in DNA replication, protein synthesis, polysaccharide biosynthesis and P53 signaling pathway. The content of TRIM59 protein in ovarian cancer was positively correlated with the infiltration of CD4+ T lymphocytes, neutrophils and NK cells. Conclusion: This study confirms that TRIM59 is highly expressed in ovarian cancer and closely related to the prognosis of ovarian cancer patients, which can be used as a new therapeutic target and diagnostic marker.

Cite this article

ZHENG Shunxin , ZHAO Maocheng , WEN Hongwei , JIANG Lifang . Analysis of TRIM59 expression and its clinical significance in ovarian cancer by integrated bioinformatics[J]. Journal of Baotou Medical College, 2025 , 41(11) : 24 -28 . DOI: 10.16833/j.cnki.jbmc.2025.11.005

References

[1] Sung H, Ferlay J, Siegel RL, et al. Global cancer statistics 2020: globocan estimates of incidence and mortality worldwide for 36 cancers in 185 countries[J]. CA Cancer J Clin, 2021, 71(3): 209-249.
[2] Menon U, Gentry-Maharaj A, Burnell M, et al. Ovarian cancer population screening and mortality after long-term follow-up in the UK Collaborative Trial of Ovarian Cancer Screening (UKCTOCS): a randomised controlled trial[J]. Lancet, 2021, 397(10290): 2182-2193.
[3] Kroeger PT Jr, Drapkin R. Pathogenesis and heterogeneity of ovarian cancer[J]. Curr Opin Obstet Gynecol, 2017, 29(1): 26-34.
[4] Hatakeyama S. TRIM family proteins: roles in autophagy, immunity, and carcinogenesis[J]. Trends Biochem Sci, 2017, 42(4): 297-311.
[5] Sideris M, Menon U, Manchanda R. Screening and prevention of ovarian cancer[J]. Med J Aust, 2024, 220(5): 264-274.
[6] Chuffa L, Reiter RJ, Lupi LA. Melatonin as a promising agent to treat ovarian cancer: molecular mechanisms[J]. Carcinogenesis, 2017, 38(10): 945-952.
[7] Ozato K, Shin DM, Chang TH, et al. TRIM family proteins and their emerging roles in innate immunity[J]. Nat Rev Immunol, 2008, 8(11): 849-860.
[8] Sang Y, Li Y, Zhang Y, et al. CDK5-dependent phosphorylation and nuclear translocation of TRIM59 promotes macroH2A1 ubiquitination and tumorigenicity[J]. Nat Commun, 2019, 10(1): 4013.
[9] Han T, Guo M, Gan M, et al. TRIM59 regulates autophagy through modulating both the transcription and the ubiquitination of BECN1[J]. Autophagy, 2018, 14(12): 2035-2048.
[10] Wang H, Lou J, Liu H, et al. TRIM59 deficiency promotes M1 macrophage activation and inhibits colorectal cancer through the STAT1 signaling pathway[J]. Sci Rep, 2024, 14(1): 16081.
[11] Wu C, Shang XQ, You ZP, et al. TRIM59 promotes retinoblastoma progression by activating the p38-MAPK signaling pathway[J]. Invest Ophthalmol Vis Sci, 2020, 61(10): 2.
[12] Aubrey BJ, Kelly GL, Janic A, et al, Strasser A. How does p53 induce apoptosis and how does this relate to p53-mediated tumour suppression[J]. Cell Death Differ, 2018, 25(1): 104-113.
[13] Kruiswijk F, Labuschagne CF, Vousden KH. p53 in survival, death and metabolic health: a lifeguard with a licence to kill[J]. Nat Rev Mol Cell Biol, 2015, 16(7): 393-405.
[14] Liu Y, Jiang N, Chen W, et al. TRIM59-mediated ferroptosis enhances neuroblastoma development and chemosensitivity through p53 ubiquitination and degradation[J]. Heliyon, 2024, 10(4): e26014.
[15] Liu R, Li H, Xu Y, et al. Blockade of TRIM59 enhances esophageal cancer cell chemosensitivity to cisplatin by upregulating p53[J]. Oncol Lett, 2021, 21(1): 6.
[16] Kärre K. NK cells, MHC class I molecules and the missing self[J]. Scand J Immunol, 2002, 55(3): 221-228.
[17] Acosta JC, Bahr JM, Basu S, et al. Expression of CISH, an inhibitor of NK cell function, increases in association with ovarian cancer development and progression[J]. Biomedicines, 2023, 11(2): 299.
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