Identification of TRIM56 as a Potential Biomarker for Lung Adenocarcinoma

Lü, Kun; Sui, Yingli; Fu, Lin

doi:10.2147/cmar.s288111

Cited by 15 publications

(14 citation statements)

References 35 publications

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“…One of the earliest clues that TRIM56 might be involved in cancer was that TRIM56 is amplified in most primary effusion leukemia (PEL) cell lines and is involved in cell signaling, metabolism and protein maturation [ 30 ]. Furthermore, TRIM56 has been shown to be an oncogene in lung and breast cancers [ 31 , 32 ], but a tumor suppressor in acute myeloid leukemia (AML). In our study, we found that TRIM56 expression was elevated in gliomas and associated with poor survival of glioma patients.…”

Section: Discussionmentioning

confidence: 99%

TRIM56 promotes malignant progression of glioblastoma by stabilizing cIAP1 protein

Zhang

Xue

et al. 2022

J Exp Clin Cancer Res

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Background The tripartite motif (TRIM) family of proteins plays a key role in the developmental growth and therapeutic resistance of many tumors. However, the regulatory mechanisms and biological functions of TRIM proteins in human glioblastoma (GBM) are not yet fully understood. In this study, we focused on TRIM56, which emerged as the most differentially expressed TRIM family member with increased expression in GBM. Methods Western blot, real-time quantitative PCR (qRT-PCR), immunofluorescence (IF) and immunohistochemistry (IHC) were used to study the expression levels of TRIM56 and cIAP1 in GBM cell lines. Co-immunoprecipitation (co-IP) was used to explore the specific binding between target proteins and TRIM56. A xenograft animal model was used to verify the tumor promoting effect of TRIM56 on glioma in vivo. Results We observed elevated expression of TRIM56 in malignant gliomas and revealed that TRIM56 promoted glioma progression in vitro and in a GBM xenograft model in nude mice. Analysis of the Human Ubiquitin Array and co-IPs showed that cIAP1 is a protein downstream of TRIM56. TRIM56 deubiquitinated cIAP1, mainly through the zinc finger domain (amino acids 21–205) of TRIM56, thereby reducing the degradation of cIAP1 and thus increasing its expression. TRIM56 also showed prognostic significance in overall survival of glioma patients. Conclusions TRIM56-regulated post-translational modifications may contribute to glioma development through stabilization of cIAP1. Furthermore, TRIM56 may serve as a novel prognostic indicator and therapeutic molecular target for GBM.

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Section: Discussionmentioning

confidence: 99%

TRIM56 promotes malignant progression of glioblastoma by stabilizing cIAP1 protein

Zhang

Xue

et al. 2022

J Exp Clin Cancer Res

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“…In recent years, studies have found that TRIM56 plays an essential role in tumorigenesis and development. The low expression of TRIM56 is related to tumour development, metastasis, and poor prognosis of lung adenocarcinoma (Lu et al, 2021), myeloma (Chen et al, 2018) and ovarian cancer(Zhao et al,2018). However, TRIM56 can up-regulate the stability of ER-α protein through ubiquitination and promote breast cancer cell proliferation (Xue et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

“…In recent years, studies have found that TRIM56 plays an essential role in tumorigenesis and development. Research proved that overexpression of TRIM56 inhibits the invasion and migration of lung adenocarcinoma cells (Lu et al, 2021). TRIM56 may inhibit the proliferation of multiple myeloma cells and induce apoptosis by activating the TLR3/TRIF signalling pathway (Chen et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

TRIM56 inhibits autophagy in esophageal cancer cells and its clinical significance

Gao

Hui

et al. 2022

Preprint

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Background: Esophageal cancer is one of the most common malignant tumors in the digestive system. Comprehensive treatment measures are mainly taken with surgery as the primary supplement to radiotherapy and chemotherapy, but the overall effect is still unsatisfactory. The tripartite motif containing 56 (TRIM56) is a family of TRIM proteins, and it has been found to play an essential role in tumorigenesis and development. We investigated the expression of TRIM56 in esophageal cancer and explored the potential regulatory role of TRIM56 in autophagy in esophageal cancer cells Eca109. Results: In this study, quantitative real-time PCR (qRT-PCR) assay, western blot (WB) and immunofluorescence (IF) were first used to detect the expression of TRIM56 in the Eca109 cells and esophageal cancer tissues. Gene chip analysis showed that the expression of autophagy-related genes LC3 and ATG12 was up-regulated, and regulated autophagy-related signal molecules PIK3CB, AKT2, and FOXO4 expression up-regulation after TRIM56 was down-regulated. Fluorescence immunoassay results showed that after TRIM56 was down-regulated, LC3BII aggregated in the cytoplasm. Conclusion: This study reveals that TRIM56 might inhibit autophagy in the Eca109 esophageal carcinoma cell line.

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“…TRIM13 over-expression in a xenograft mouse model inhibited tumor growth and induced apoptosis in vivo, and the possible mechanism was to inhibit cell proliferation and induce apoptosis by regulating the nuclear factor kappa B (NF-κB) pathway (Xu et al, 2019). The expression of TRIM56 in lung adenocarcinoma (LUAD) was reduced and associated with a poor prognosis, and the over-expression of TRIM56 inhibited the invasion and migration of LUAD cells (Lu et al, 2021). TRIM72 inhibited tumor progression and stress granule formation by modulating oncogenic protein G3BP2 activity in NSCLC (Li et al, 2021a), which is a potential therapeutic target.…”

Section: The Tripartite Motifs Protein Family In Lung Cancermentioning

confidence: 99%

Research progress of TRIMs protein family in tumors

HUANG¹,

WU²,

LIU³

et al. 2023

Biocell

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The tripartite motif (TRIMs) protein family has E3 ubiquitin ligase activity among most of its members. They participate in multiple cellular processes and signaling pathways in living organisms, including cell cycle, growth, and metabolism, and mediate chromatin modification, transcriptional regulation, post-translational modification, and cellular autophagy. Previous studies have confirmed that the TRIMs protein family is involved in the development of various cancers and correlated with the prognosis of tumor patients. Here we summarize the biological roles of the TRIMs protein family in cancers.

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Identification of TRIM56 as a Potential Biomarker for Lung Adenocarcinoma

Cited by 15 publications

References 35 publications

TRIM56 promotes malignant progression of glioblastoma by stabilizing cIAP1 protein

TRIM56 promotes malignant progression of glioblastoma by stabilizing cIAP1 protein

TRIM56 inhibits autophagy in esophageal cancer cells and its clinical significance

Research progress of TRIMs protein family in tumors

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