TRIM23 overexpression is a poor prognostic factor and contributes to carcinogenesis in colorectal cancer

Han, Yudong; Tan, Ye; Zhao, Yuanyuan; Zhang, Yongchun; He, Xueling; Li, Yu; Jiang, Haiping; Lü, Haijun; Tian, Haiying

doi:10.1111/jcmm.15203

Cited by 29 publications

(29 citation statements)

References 31 publications

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“…At the same time, MDM2 is targeted by p53 to form a negative feedback loop for the dynamic regulation of p53 under stressed and unstressed conditions [177]. RCHY1, COP1, CHIP, HUWE1, RING1, FBXW7, Synoviolin, MKRN1, TOPORS, CARP1/2, CUL4a-DDB1-ROC, CUL5, RNF115, TRIM23, TRIM24, TRIM28, TRIM39, TRIM69, TRIM71 can also target p53 for K48-linked polyubiquitination and degradation [178][179][180][181][182][183][184][185]. K48linked polyubiquitination of p53 can be regulated by various molecules.…”

Section: Ubiquitination Of P53mentioning

confidence: 99%

The role of ubiquitination and deubiquitination in cancer metabolism

Sun¹,

Liu²,

Yang³

2020

Mol Cancer

281

178

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Metabolic reprogramming, including enhanced biosynthesis of macromolecules, altered energy metabolism, and maintenance of redox homeostasis, is considered a hallmark of cancer, sustaining cancer cell growth. Multiple signaling pathways, transcription factors and metabolic enzymes participate in the modulation of cancer metabolism and thus, metabolic reprogramming is a highly complex process. Recent studies have observed that ubiquitination and deubiquitination are involved in the regulation of metabolic reprogramming in cancer cells. As one of the most important type of post-translational modifications, ubiquitination is a multistep enzymatic process, involved in diverse cellular biological activities. Dysregulation of ubiquitination and deubiquitination contributes to various disease, including cancer. Here, we discuss the role of ubiquitination and deubiquitination in the regulation of cancer metabolism, which is aimed at highlighting the importance of this post-translational modification in metabolic reprogramming and supporting the development of new therapeutic approaches for cancer treatment.

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Section: Ubiquitination Of P53mentioning

confidence: 99%

The role of ubiquitination and deubiquitination in cancer metabolism

Sun¹,

Liu²,

Yang³

2020

Mol Cancer

281

178

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“…Multiple TRIM proteins have been identified and most of them homodimerize through their coiled-coil domain [318,319]. As these proteins are overexpressed in many tumors they are hypothesized to contribute to tumorigenesis [320,321]. For instance, increased TRIM23 expression is correlated with a poor prognosis in colorectal cancer [321] and lung adenocarcinoma [322].…”

Section: Trimmentioning

confidence: 99%

Mechanisms of TP53 Pathway Inactivation in Embryonic and Somatic Cells—Relevance for Understanding (Germ Cell) Tumorigenesis

Timmerman

Remmers

Hillenius

et al. 2021

IJMS

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The P53 pathway is the most important cellular pathway to maintain genomic and cellular integrity, both in embryonic and non-embryonic cells. Stress signals induce its activation, initiating autophagy or cell cycle arrest to enable DNA repair. The persistence of these signals causes either senescence or apoptosis. Over 50% of all solid tumors harbor mutations in TP53 that inactivate the pathway. The remaining cancers are suggested to harbor mutations in genes that regulate the P53 pathway such as its inhibitors Mouse Double Minute 2 and 4 (MDM2 and MDM4, respectively). Many reviews have already been dedicated to P53, MDM2, and MDM4, while this review additionally focuses on the other factors that can deregulate P53 signaling. We discuss that P14ARF (ARF) functions as a negative regulator of MDM2, explaining the frequent loss of ARF detected in cancers. The long non-coding RNA Antisense Non-coding RNA in the INK4 Locus (ANRIL) is encoded on the same locus as ARF, inhibiting ARF expression, thus contributing to the process of tumorigenesis. Mutations in tripartite motif (TRIM) proteins deregulate P53 signaling through their ubiquitin ligase activity. Several microRNAs (miRNAs) inactivate the P53 pathway through inhibition of translation. CCCTC-binding factor (CTCF) maintains an open chromatin structure at the TP53 locus, explaining its inactivation of CTCF during tumorigenesis. P21, a downstream effector of P53, has been found to be deregulated in different tumor types. This review provides a comprehensive overview of these factors that are known to deregulate the P53 pathway in both somatic and embryonic cells, as well as their malignant counterparts (i.e., somatic and germ cell tumors). It provides insights into which aspects still need to be unraveled to grasp their contribution to tumorigenesis, putatively leading to novel targets for effective cancer therapies.

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“…The majority of tumor promoting TRIMs belong to the p53 negative regulatory TRIMs either through an increased polyubiquitination and subsequent proteasomal degradation or, alternatively, by hindering p53 from entering the nucleus and thereby impairing its transcriptional activity. P53 inhibitory TRIM members which are characteristically overexpressed in CRC include TRIM23 [ 58 ], TRIM24 [ 59 ], TRIM25 [ 62 ], TRIM28 [ 67 , 69 ], and TRIM29 [ 70 ]. TRIM23 is significantly overexpressed in CRC, a characteristic associated with poor patient survival.…”

Section: Diverse Oncogenic Signaling Pathways Are Affected By Trimmentioning

confidence: 99%

“…TRIM23 is significantly overexpressed in CRC, a characteristic associated with poor patient survival. Gene set enrichment analysis (GSEA) furthermore revealed that p53 and cell cycle signaling pathways related genes were enriched in patients with high TRIM23 levels [ 58 ]. Mechanistically, TRIM23 promotes proliferation of tumor cells mainly through an augmentation in p53 ubiquitination.…”

Section: Diverse Oncogenic Signaling Pathways Are Affected By Trimmentioning

confidence: 99%

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Multifaceted Roles of TRIM Proteins in Colorectal Carcinoma

Eberhardt

Haeussler

Nasrullah

et al. 2020

IJMS

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Colorectal cancer (CRC) is one of the most frequently diagnosed tumor in humans and one of the most common causes of cancer-related death worldwide. The pathogenesis of CRC follows a multistage process which together with somatic gene mutations is mainly attributed to the dysregulation of signaling pathways critically involved in the maintenance of homeostasis of epithelial integrity in the intestine. A growing number of studies has highlighted the critical impact of members of the tripartite motif (TRIM) protein family on most types of human malignancies including CRC. In accordance, abundant expression of many TRIM proteins has been observed in CRC tissues and is frequently correlating with poor survival of patients. Notably, some TRIM members can act as tumor suppressors depending on the context and the type of cancer which has been assessed. Mechanistically, most cancer-related TRIMs have a critical impact on cell cycle control, apoptosis, epithelial–mesenchymal transition (EMT), metastasis, and inflammation mainly through directly interfering with diverse oncogenic signaling pathways. In addition, some recent publications have emphasized the emerging role of some TRIM members to act as transcription factors and RNA-stabilizing factors thus adding a further level of complexity to the pleiotropic biological activities of TRIM proteins. The current review focuses on oncogenic signaling processes targeted by different TRIMs and their particular role in the development of CRC. A better understanding of the crosstalk of TRIMs with these signaling pathways relevant for CRC development is an important prerequisite for the validation of TRIM proteins as novel biomarkers and as potential targets of future therapies for CRC.

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TRIM23 overexpression is a poor prognostic factor and contributes to carcinogenesis in colorectal cancer

Cited by 29 publications

References 31 publications

The role of ubiquitination and deubiquitination in cancer metabolism

The role of ubiquitination and deubiquitination in cancer metabolism

Mechanisms of TP53 Pathway Inactivation in Embryonic and Somatic Cells—Relevance for Understanding (Germ Cell) Tumorigenesis

Multifaceted Roles of TRIM Proteins in Colorectal Carcinoma

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