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The TRIM proteins in cancer: from expression to emerging regulatory mechanisms

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Abstract

New clinical evidence suggests that dysregulation of the ubiquitin-mediated destruction of tumor suppressors or oncogene products is probably engaged in the etiology of leukemia and carcinoma. The superfamily of tripartite motif (TRIM)-containing protein family is among the biggest recognized single protein RING finger E3 ubiquitin ligases that are considered vital carcinogenesis regulators, which is not shocking since TRIM proteins are engaged in various biological processes, including cell growth, development, and differentiation; hence, TRIM proteins’ alterations may influence apoptosis, cell proliferation, and transcriptional regulation. In this review article, the various mechanisms through which TRIM proteins exert their role in the most prevalent malignancies including lung, prostate, colorectal, liver, breast, brain cancer, and leukemia are summarized.

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Abbreviations

ADC:

Adenocarcinoma

APL:

Acute promyelocytic leukemia

BRAF:

B-Raf proto-oncogene serine/threonine-protein kinase

TRIM:

The superfamily of tripartite motif-containing proteins

ISG15:

IFN-stimulated protein of 15

PML:

Promyelocytic leukemia gene

SUMO:

Small ubiquitin-like modifier

RET:

Rearranged during transfection

NSCLC:

Non-small cell lung cancer

SCLC:

Small cell lung cancer

LCC:

Large cell carcinoma

SCC:

Squamous cell carcinoma

Mdm2:

Mouse double minute 2 homolog

STAT3:

Signal transducer and activator of transcription 3

TNBC:

Triple-negative breast cancer

Nrf2:

Nuclear factor erythroid 2–related factor 2

GBM:

Glioblastoma

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Authors and Affiliations

  1. Department of Genetics Islamic, Azad University of Marand, Marand, Iran

    A. Mohammadi

  2. Kashan University of Medical Sciences, Kashan, Iran

    M. S. Pour Abbasi

  3. Tehran University of Medical Sciences, Tehran, Iran

    S. Khorrami

  4. Department of Microbiology, Shahr-e-Qods Branch, Islamic Azad University, Tehran, Iran

    S. Khodamoradi

  5. Department of Medicine, School of Medicine, Qazvin University of Medical Sciences, Qazvin, Iran

    Z. Mohammadi Goldar

  6. Department of Internal Medicine, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

    F. Ebrahimzadeh

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AM and FE contributed to the idea design and literature search. SeK wrote parts of the manuscript. AM contributed to designing the figures. ZM contributed in language editing and writing of manuscript. MP and SaK performed the revision.

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Correspondence to F. Ebrahimzadeh.

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Mohammadi, A., Pour Abbasi, M.S., Khorrami, S. et al. The TRIM proteins in cancer: from expression to emerging regulatory mechanisms. Clin Transl Oncol 24, 460–470 (2022). https://doi.org/10.1007/s12094-021-02715-5

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