TRIM3 and TRIM16 as potential tumor suppressors in breast cancer patients

Roshanazadeh, Mohammad Reza; Adelipour, Maryam; Sanaei, Arash; Chenane, Hadi; Rashidi, Mojtaba

doi:10.1186/s13104-022-06193-y

Cited by 6 publications

(2 citation statements)

References 35 publications

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“…The existence of B-BOX2 is a distinguishing feature of RBCC (TRIM) proteins. While the specific work of the CC domain has yet to be fully clarified, it is known to be embroiled in mRNA regulation (Roshanazadeh et al 2022 ). The NHL domain, positioned at the C-terminus of the TRIM3 protein, derives its name from NCL-1/HT2A/LIN-41, the original protein designation.…”

Section: The Structure and Biological Function Of Trim3mentioning

confidence: 99%

Advances in the antitumor mechanisms of tripartite motif-containing protein 3

Teng,

Ling,

Liu

et al. 2024

J Cancer Res Clin Oncol

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The tripartite motif-containing (TRIM) protein family has steadily become a hotspot in tumor-related research. As a member of the E3 ubiquitin ligase family, TRIM is working on many crucial biological processes, including the regulation of tumor cell proliferation, metastasis, apoptosis, and autophagy. Among the diverse TRIM superfamily members, TRIM3 operates via different mechanisms in various types of tumors. This review primarily focuses on the current state of research regarding the antitumor mechanisms of TRIM3 in different cancers. A more in-depth study of TRIM3 may provide new directions for future antitumor treatments. Our review focuses on TRIM3 proteins and cancer. We searched for relevant articles on the mechanisms by which TRIM3 affects tumorigenesis and development from 1997 to 2023 and summarized the latest progress and future directions. Triad-containing motif protein 3 (TRIM3) is an important protein, which plays a key role in the process of tumorigenesis and development. The comprehensive exploration of TRIM3 is anticipated to pave the way for future advancements in antitumor therapy, which is expected to be a new hallmark for cancer detection and a novel target for drug action. TRIM3 is poised to become a significant milestone in cancer detection and a promising focal point for drug intervention. Recent years have witnessed notable progress in research aimed at unraveling the antitumor mechanism of TRIM3, with far-reaching implications for practical tumor diagnosis, treatment protocols, efficacy evaluation, economics, and pharmaceutical utilization.

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Section: The Structure and Biological Function Of Trim3mentioning

confidence: 99%

Advances in the antitumor mechanisms of tripartite motif-containing protein 3

Teng,

Ling,

Liu

et al. 2024

J Cancer Res Clin Oncol

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“…Tripartite motif-containing protein 16 (Trim16), a member of the Trim family, has E3 ubiquitin ligase activity and serves an important role in certain diseases, such as pathological cardiac hypertrophy ( 16 ) and breast cancer ( 17 ). Receptor interacting protein kinase 2 (RIP2) belongs to the tyrosine kinase-like family ( 18 ).…”

Section: Introductionmentioning

confidence: 99%

Saikosaponin A protects against uremic toxin indole‑3 acetic acid‑induced damage to the myocardium

Chen

2023

Mol Med Rep

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Chronic kidney disease (CKD)-associated cardiac injury is a common complication in patients with CKD. Indole-3 acetic acid (IAA) is a uremic toxin that injures the cardiovascular system. Saikosaponin A (SSA) protects against pressure overload-induced cardiac fibrosis. However, the role and molecular mechanisms of IAA and SSA in CKD-associated cardiac injury remain unclear. The present study investigated the effects of IAA and SSA on CKD-associated cardiac injury in neonatal mouse cardiomyocytes and a mouse model of CKD. The expression of tripartite motif-containing protein 16 (Trim16), receptor interacting protein kinase 2 (RIP2) and phosphorylated-p38 were assessed using western blotting. The ubiquitination of RIP2 was measured by coimmunoprecipitation, and mouse cardiac structure and function were evaluated using hematoxylin and eosin staining and echocardiography. The results demonstrated that, SSA inhibited IAA-induced cardiomyocyte hypertrophy, upregulated Trim16 expression, downregulated RIP2 expression and decreased p38 phosphorylation. Furthermore, Trim16 mediated SSA-induced degradation of RIP2 by ubiquitination. In a mouse model of IAA-induced CKD-associated cardiac injury, SSA upregulated the protein expression levels of Trim16 and downregulated those of RIP2. Moreover, SSA alleviated heart hypertrophy and diastolic dysfunction in IAA-treated mice. Taken together, these results suggest that SSA is a protective agent against IAA-induced CKD-associated cardiac injury and that Trim16-mediated ubiquitination-related degradation of RIP2 and p38 phosphorylation may contribute to the development of CKD-associated cardiac injury.

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LncRNA OTUD6B-AS1 overexpression promoted GPX4-mediated ferroptosis to suppress radioresistance in colorectal cancer

Zhang

Lin

et al. 2023

Clin Transl Oncol

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TRIM3 and TRIM16 as potential tumor suppressors in breast cancer patients

Cited by 6 publications

References 35 publications

Advances in the antitumor mechanisms of tripartite motif-containing protein 3

Advances in the antitumor mechanisms of tripartite motif-containing protein 3

Saikosaponin A protects against uremic toxin indole‑3 acetic acid‑induced damage to the myocardium

LncRNA OTUD6B-AS1 overexpression promoted GPX4-mediated ferroptosis to suppress radioresistance in colorectal cancer

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