The tripartite motif (TRIM) family proteins play a great role in carcinogenesis. However, the expression pattern, prognostic value and biological functions of tripartite motif containing 23 (TRIM23) in colorectal cancer (CRC) are poorly understood. Here, we found that TRIM23 is up-regulated and associated with tumour size, lymph node metastasis, American Joint Committee on Cancer (AJCC) stage and poor prognosis in CRC. Multivariate Cox regression analyses revealed that TRIM23 overexpression could be identified as an independent prognostic factor for CRC. TRIM23 could promote the proliferation of CRC cell in vitro and in vivo; additionally, TRIM23 depletion induced G1-phase arrest. Gene set enrichment analysis (GSEA) revealed that P53 and cell cycle signalling pathway-related genes were enriched in patients with high TRIM23 expression levels. We show in this study that TRIM23 physically binds to P53 and enhances the ubiquitination of P53, thereby promoting tumour proliferation. Thus, our data indicated that TRIM23 acts as an oncogene in colorectal carcinogenesis and may provide a novel therapeutic target for CRC management.
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http://dx.doi.org/10.1111/jcmm.15203 | DOI Listing |
Apoptosis
December 2024
Department of Oncology, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, 213003, China.
5-Fluorouracil (5-FU) is one of the most common chemotherapeutic agents for colorectal cancer (CRC), but its application is often limited by resistance. Tripartite motif containing 23 (TRIM23) has been reported to be dysregulated in various tumors and involved in tumor progression and chemotherapy resistance. However, its relationship with CRC 5-FU resistance and the underlying mechanism are still unclear.
View Article and Find Full Text PDFHum Pathol
October 2024
Department of Pathology, School of Basic Medical Sciences and Qilu Hospital, Shandong University, Jinan, China. Electronic address:
EMBO J
July 2024
Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Energy stress, characterized by the reduction of intracellular ATP, has been implicated in various diseases, including cancer. Here, we show that energy stress promotes the formation of P-bodies in a ubiquitin-dependent manner. Upon ATP depletion, the E3 ubiquitin ligase TRIM23 catalyzes lysine-63 (K63)-linked polyubiquitination of HCLS1-associated protein X-1 (HAX1).
View Article and Find Full Text PDFJ Cell Biochem
April 2024
Laboratory of Molecular Oncology, Centre for DNA Fingerprinting and Diagnostics, Hyderabad, Telangana, India.
Missense mutations in the DNA binding domain of p53 are observed frequently in esophageal squamous cell carcinoma (ESCC). Recent studies have revealed the potentially oncogenic transcriptional networks regulated by mutant p53 proteins. However, majority of these studies have focused on common "hotspot" p53 mutations while rarer mutations are poorly characterized.
View Article and Find Full Text PDFDev Comp Immunol
February 2024
College of Animal Science and Technology, Northeast Agricultural University, Harbin, 150030, PR China. Electronic address:
TRIM proteins play a crucial antiviral effector role in the innate immune system of vertebrates. In this study, we found that TRIM proteins exhibited the highest expression levels in immune organs such as spleen and kidney during IHNV infection in rainbow trout, meanwhile, we successfully amplified TRIM23 and TRIM32 from diseased rainbow trout and analyzed their gene sequences, revealing that rainbow trout TRIM23 and TRIM32 proteins are closely related to Atlantic salmon and Chinook salmon; In this experiment, the TRIM23 and TRIM32 protein genes were resoundingly constructed as a recombinant plasmids and expressed in CHSE-214 cells. Upon transfected with the recombinant plasmid, followed by viral infection, significant decreasion in the copy numbers of the virus was observed, indicating that the TRIM23 and TRIM32 proteins of rainbow trout play an important role in inhibiting virus replication, with the TRIM32 role being the most pronounced.
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