SavedAdd your journal

Journals / Muğla Sıtkı Koçman Üniversitesi Tıp Dergisi / 2026 / Volume: 12 Issue: 1

An Investigation of TRIM36 Expression in Breast Cancer

Meme Kanserinde TRIM36 Ekspresyonunun İncelenmesi

Aycan Çelik(ZONGULDAK BÜLENT ECEVİT ÜNİVERSİTESİ)0000-0003-0151-4081
Sevim Karakaş Çelik(ZONGULDAK BÜLENT ECEVİT ÜNİVERSİTESİ, TIP FAKÜLTESİ)0000-0003-0505-7850
Güldeniz Karadeniz Çakmak(ZONGULDAK BÜLENT ECEVİT ÜNİVERSİTESİ, TIP FAKÜLTESİ)0000-0001-5802-4441
Fürüzan Köktürk(ZONGULDAK BÜLENT ECEVİT ÜNİVERSİTESİ, TIP FAKÜLTESİ)0000-0002-2580-7770
Pages
—
Publication Date
2025-04-30
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Although this study suggests that TRIM36 gene expression levels in breast cancer tissues do not differ from normal tissues, the limited sample size highlights the need for more comprehensive studies to elucidate the relationship between the TRIM36 gene and breast cancer.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Breast cancer is the most frequently diagnosed cancer type worldwide and ranks 2nd among cancers that cause death.
📊
Key Findings & Data:While the role of TRIM36 has been investigated in certain human cancers, such as prostate and lung cancer, its functions remain largely unexplored.
💡
Conclusion & Impact:Although this study suggests that TRIM36 gene expression levels in breast cancer tissues do not differ from normal tissues, the limited sample size highlights the need for more comprehensive studies to elucidate the relationship between the TRIM36 gene and breast cancer.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Gene Expression · Breast Cancer · TRIM36

Abstract

Breast cancer is the most frequently diagnosed cancer type worldwide and ranks 2nd among cancers that cause death. While the role of TRIM36 has been investigated in certain human cancers, such as prostate and lung cancer, its functions remain largely unexplored. In this study, the expression level of TRIM36, whose role in breast cancer has not been previously examined, and its potential association with breast cancer pathogenesis were analyzed. RNA was isolated from normal and tumor tissues of 45 breast cancer patients. Complementary DNA (cDNA) was synthesized from the RNA, and mRNA expression levels of GAPDH and TRIM36 were quantified using qRT-PCR. TRIM36 expression was observed in breast tissues; however, no statistically significant difference was found in TRIM36 mRNA expression levels, normalized to GAPDH, between normal and tumor tissues (p=0.731). Although this study suggests that TRIM36 gene expression levels in breast cancer tissues do not differ from normal tissues, the limited sample size highlights the need for more comprehensive studies to elucidate the relationship between the TRIM36 gene and breast cancer.

Özet

Meme kanseri, dünya genelinde en sık teşhis edilen kanser türü olup, kansere bağlı ölümler arasında ikinci sırada yer almaktadır. TRIM36’nın rolü prostat ve akciğer kanseri gibi bazı insan kanserlerinde araştırılmış olsa da bu proteinin işlevleri büyük ölçüde bilinmemektedir. Bu çalışmada, daha önce meme kanseri ile ilişkisi incelenmemiş olan TRIM36’nın ifade düzeyi ve meme kanseri patogeneziyle potansiyel ilişkisi analiz edilmiştir. Çalışma kapsamında, 45 meme kanseri hastasının normal ve tümör dokularından RNA izole edilmiştir. İzole edilen RNA'dan tamamlayıcı DNA (cDNA) sentezlenmiş ve GAPDH ile TRIM36’nın mRNA ifade düzeyleri qRT-PCR yöntemiyle ölçülmüştür. TRIM36 ifadesinin meme dokularında gözlendiği tespit edilmiştir; ancak, GAPDH’ye normalize edilen TRIM36 mRNA ifade düzeyleri açısından normal ve tümör dokuları arasında istatistiksel olarak anlamlı bir fark bulunamamıştır (p=0.731). Bu çalışma, meme kanseri dokularında TRIM36 gen ifadesinin normal dokulardan farklı olmadığını öne sürse de sınırlı örneklem boyutu, TRIM36 geni ile meme kanseri arasındaki ilişkinin daha kapsamlı çalışmalarla aydınlatılması gerekliliğini ortaya koymaktadır.

🔖

Cite This Article

Çelik, A., Çelik, S. K., Çakmak, G. K., Köktürk, F. (2025). An Investigation of TRIM36 Expression in Breast Cancer. Muğla Sıtkı Koçman Üniversitesi Tıp Dergisi, Volume: 12 Issue: 1. https://doi.org/10.47572/muskutd.1600240

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (38)

  1. Bray F, Ferlay J, Soerjomataram I, et al. GLOBOCAN estimates of cancer incidence and mortality worldwide for 2022. GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA: CA Cancer J Clin, 2024;74(3):229–63.
  2. Zhou W, Zhang Y, Zhong C, et al. Decreased expression of TRIM21 indicates unfavorable outcome and promotes cell growth in breast cancer. Cancer Manag Res. 2018;10:3687-97.
  3. Hatakeyama S. TRIM family proteins: Roles in autophagy, immunity, and carcinogenesis. Trends Biochem Sci, 2017; 42(4):297–311.
  4. Hatakeyama S. TRIM proteins and cancer. Nat Rev Cancer. 2011;11(11):792.
  5. Reymond A, Meroni G, Fantozzi A, et al. The tripartite motif family identifies cell compartments. EMBO J. 2001;20(9):2140-51.
  6. Short KM, Cox TC. Subclassification of the RBCC/TRIM superfamily reveals a novel motif necessary for microtubule binding. J Biol Chem. 2006;281(13):8970–80.
  7. Watanabe M, Hatakeyama S. TRIM proteins and diseases. J Biochem. 2017; 1;161(2):135-44.
  8. Goddard AD, Borrow J, Freemont PS, Solomon E. Characterization of a zinc finger gene disrupted by the t(15;17) in acute promyelocytic leukemia. Science. 1991;29;254(5036):1371-4.
  9. Fang YY, Li JL, Ding H, et al Regulation of TRIM24 by miR-511 modulates cell proliferation in gastric cancer. J Exp Clin Cancer Res. 2017;23:36(1):17.
  10. Groner AC, Cato L, de Tribolet-Hardy J, et al. TRIM24 Is an Oncogenic Transcriptional Activator in Prostate Cancer. Cancer Cell. 2016:13;29(6):846-58.
  11. Appikonda S, Thakkar KN, Freeman WM. Regulation of gene expression in human cancers by TRIM24. Drug Discov Today Technol. 2016:19:57-63.
  12. Obad S, dos Santos CO, Petri A, et al. Regulation of the interferon-inducible p53 target gene TRIM22 (Staf50) in human T lymphocyte activation. J Interferon Cytokine Res. 2007:27(10):857-64.
  13. Joo, HM, Kim JY, Jeong JB, et al. Ret finger protein 2 enhances ionizing radiation-induced apoptosis via degradation of AKT and MDM2. Eur J Cell Biol. 2011:90(5);420-31.
  14. Qiu F, Xiong JP, Deng J, et al. TRIM29 functions as an oncogene in gastric cancer and is regulated by miR-185. Int J Clin Exp Pathol. 2015;8(5):5053-61.
  15. Micale L, Chaignat E, Merla G. TRIM8 downregulation in glioma affects cell proliferation and it is associated with patients survival. BMC Cancer. 2015;15(6):470.
  16. Okumura F, Matsunaga Y, Katayama Y, et al. TRIM8 modulates STAT3 activity through negative regulation of PIAS3. J Cell Sci. 2010;123(Pt 13):2238-45.
  17. Balint I, Müller A, Nagy A, et al. Cloning and characterisation of the RBCC728/TRIM36 zinc-binding protein from the tumor suppressor gene region at chromosome 5q22.3. Gene. 2004;332(5):45-50.
  18. Miyajima N, Maruyama S, Kasai H, et al. TRIM36 interacts with the kinetochore protein CENP-H and delays cell cycle progression. Biochem Biophys Res Commun. 2009;381(3):383–7.
  19. Koressaar T, Remm M. Enhancements and modifications of primer design program Primer3. Bioinformatics. 2007;23(10):1289-91.
  20. Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. Methods. 2001;25(4):402-8.
  21. Ikeda K, Orimo A, Higashi Y, et al. Efp as a primary estrogen-responsive gene in human breast cancer. FEBS Lett. 2000;472(1):9-13.
  22. Urano T, Saito T, Tsukui T, et al. Efp targets 14- 3-3 sigma for proteolysis and promotes breast tumour growth. Nature. 2002;417(6891):871–5.
  23. Chambon M, Orsetti B, Berthe ML, et al. Prognostic significance of TRIM24/TIF-1α gene expression in breast cancer. Am J Pathol. 2011;178(4):1461-9.
  24. Yuan Z, Villagra A, Peng L, et al. The ATDC (TRIM29) protein binds p53 and antagonizes p53-mediated functions. Mol Cell Biol. 2010;30(12):3004–15.
  25. Wang L, Heidt DG, Lee CJ, et al. Oncogenic function of ATDC in pancreatic cancer through Wnt pathway activation and beta-catenin stabilization. Cancer Cell. 2009;15(3):207–19.
  26. Liu J, Welm B, Boucher KM, et al. TRIM29 functions as a tumor suppressor in nontumorigenic breast cells and invasive ER+ breast cancer. Am J Pathol. 2012;180(2):839-47.
  27. Wang Y, Liu C, Xie Z, et al. Knockdown of TRIM47 inhibits breast cancer tumorigenesis and progression through the inactivation of PI3K/Akt pathway. Chem Biol Interact. 2020;317:108960.
  28. Cao J, Yang M, Guo D, et al. Emerging roles of tripartite motif family proteins (TRIMs) in breast cancer. Cancer Med. 2024;13(14):e7472.
  29. Zheng M, Wang J, Ling L, et al. Screening and analysis of breast cancer genes regulated by the human mammary microenvironment in a humanized mouse model. Oncol Lett. 2016;12(6):5261-8.
  30. Kimura N, Yamada Y, Takayama KI, et al. Androgen-responsive tripartite motif 36 enhances tumor-suppressive effect by regulating apoptosis-related pathway in prostate cancer. Cancer Sci. 2018;109(12):3840-52.
  31. Liang C, Wang S, Qin C, et al. TRIM36, a novel androgen-responsive gene, enhances anti-androgen efficacy against prostate cancer by inhibiting MAPK/ERK signaling pathways. Cell Death Dis. 2018;9(2):1-13.
  32. Zhan W, Han T, Zhang C, et al. TRIM59 promotes the proliferation and migration of non-small cell lung cancer cells by upregulating cell cycle-related proteins. PLoS One. 2015;10(11):e0142596.
  33. Zhang H, Sun W, Qiao G, et al. The expression of tripartite motif protein 36 and β-catenin correlates with the prognosis of esophageal cancer. Gastroenterol Res Pract. 2020;2020(7641761):1-9.
  34. Olsson M, Beck S, Kogner P, et al. Genome-wide methylation profiling identifies novel methylated genes in neuroblastoma tumors. Epigenetics. 2016;11(1):74-84.
  35. Zhao X, Zhou T, Wang Y, et al. TRIM36 regulates neuroendocrine differentiation of prostate cancer via HK2 ubiquitination and GPx4 deficiency. Res Sq. 2022;Version 1:e2190616.
  36. Liu X, Yan C, Chang C, et al. FOXA2 Suppression by TRIM36 Exerts Anti-Tumor Role in Colorectal Cancer Via Inducing NRF2/GPX4-Regulated Ferroptosis. Adv Sci (Weinh). 2023;10(35):e2304521.
  37. Jiang M, Ma Y, Chen C, et al. Androgen-responsive gene database: integrated knowledge on androgen-responsive genes. Mol Endocrinol. 2009;23(11):1927-33.
  38. Labrie F, Simard J, de Launoit Y, et al. Androgens and breast cancer. Cancer Detect Prev. 1992;16(1):31-8.