Effect of EI24 expression on the tumorigenesis of Apc colorectal cancer mouse model

Nam, Tae Wook; Park, Song Yi; Lee, Jae Hoon; Roh, Jae Il; Lee, Han Woong

doi:10.1016/j.bbrc.2019.04.186

Cited by 3 publications

(4 citation statements)

References 26 publications

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“…The human EI24 gene is located on chromosome 11q23, where heterozygote deficiency occurs in a variety of malignant tumors, leading to the decrease or disappearance of its anti-cancer function (20). Abnormalities in EI24 expression are closely associated with the occurrence and progression of tumors (21)(22)(23). In addition, our previous study confirmed EI24 as the target molecule of miR-483, using reporter gene detection (24).…”

Section: Mir-483 Promotes the Development Of Colorectal Cancer By Inh...supporting

confidence: 63%

“…Our previous studies reported that the expression level of miR-483 was increased in esophageal squamous cell carcinoma, and that upregulation of miR-483 could promote the development of esophageal cancer (24,28). Furthermore, a reporter gene test confirmed that EI24 was the target molecule of miR-483 (21). In the current experiment, the expression level of EI24 in miR-483 overexpressing stable Caco-2 cells and in the NC group was detected using RT-qPCR.…”

Section: Ei24 Expression Is Associated With Patient Prognosissupporting

confidence: 54%

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miR‑483 promotes the development of colorectal cancer by inhibiting the expression level of EI24

Zhou

Yang

et al. 2021

Mol Med Rep

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MicroRNAs (miRs) serve an important role in cell differentiation, proliferation and apoptosis by negatively regulating gene expression at the transcriptional or post-transcriptional level. EI24 autophagy associated transmembrane protein (EI24) is a tumor suppressor gene that serves an important role in the occurrence and development of digestive system tumors. However, little is known regarding the relationship between EI24 and the prognosis of patients with colorectal cancer (CRC). Our previous study confirmed EI24 as the target molecule of miR-483, using reporter gene detection. Thus, the aim of the present study was to elucidate the effect of the abnormal expression of miR-483 on the malignant phenotype of CRC through a series of cell function experiments and nude mice tumorigenicity experiments, and to determine the expression level of EI24, a downstream target gene of miR-483, in CRC and its relationship with patient prognosis. In CRC tissues and cells, the expression level of miR-483 was upregulated, while the expression level of EI24 was downregulated. Cell function tests such as MTT assay, cell cycle assay, colony formation assay, Migration and invasion assays and nude mice tumorigenicity experiments demonstrated that the overexpression of miR-483 promoted the proliferation, invasion and metastasis of CRC. Moreover, the reverse transcription-quantitative PCR results indicated that overexpression of miR-483 inhibited the expression level of EI24. The relationship between the clinical data and immunohistochemical results from 183 patients with CRC and survival was examined. It was found that the expression level of EI24 was positively associated with the prognosis of patients. As a cancer-promoting factor, miR-483 enhances the proliferation, migration and invasion of CRC cells by reducing the expression level of EI24.

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Section: Mir-483 Promotes the Development Of Colorectal Cancer By Inh...supporting

confidence: 63%

Section: Ei24 Expression Is Associated With Patient Prognosissupporting

confidence: 54%

miR‑483 promotes the development of colorectal cancer by inhibiting the expression level of EI24

Zhou

Yang

et al. 2021

Mol Med Rep

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“…EI24 is an important autophagy-associated protein and tumor suppressor that has been found to be under expressed in a variety of malignancies [ 90 , 91 , 92 , 93 ], although other studies have found no correlation or even positive correlation between EI24 expression and tumorigenesis in certain cancers, indicating that effects of EI24 depend on the cellular context of the cancers [ 94 , 95 ]. Additionally, EI24 regulates the UPS by targeting certain RING E3 ligases for autophagy mediated degradation; earlier studies have identified 161 RING E3 ligases as potential targets of EI24, the best characterized of which are TNFR-associated factor 2/5 (TRAF2/5), mouse double minute 2 homolog (MDM2), and tripartite motif containing 41 (TRIM41)—also called RING finger protein that interacts with C kinase 1 (RINCK1) [ 94 , 96 ].…”

Section: Molecular Components In the Intersections Of Ups And Autopha...mentioning

confidence: 99%

Intersections of Ubiquitin-Proteosome System and Autophagy in Promoting Growth of Glioblastoma Multiforme: Challenges and Opportunities

Visintin

Ray

2022

Cells

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Glioblastoma multiforme (GBM) is a brain tumor notorious for its propensity to recur after the standard treatments of surgical resection, ionizing radiation (IR), and temozolomide (TMZ). Combined with the acquired resistance to standard treatments and recurrence, GBM is an especially deadly malignancy with hardly any worthwhile treatment options. The treatment resistance of GBM is influenced, in large part, by the contributions from two main degradative pathways in eukaryotic cells: ubiquitin-proteasome system (UPS) and autophagy. These two systems influence GBM cell survival by removing and recycling cellular components that have been damaged by treatments, as well as by modulating metabolism and selective degradation of components of cell survival or cell death pathways. There has recently been a large amount of interest in potential cancer therapies involving modulation of UPS or autophagy pathways. There is significant crosstalk between the two systems that pose therapeutic challenges, including utilization of ubiquitin signaling, the degradation of components of one system by the other, and compensatory activation of autophagy in the case of proteasome inhibition for GBM cell survival and proliferation. There are several important regulatory nodes which have functions affecting both systems. There are various molecular components at the intersections of UPS and autophagy pathways that pose challenges but also show some new therapeutic opportunities for GBM. This review article aims to provide an overview of the recent advancements in research regarding the intersections of UPS and autophagy with relevance to finding novel GBM treatment opportunities, especially for combating GBM treatment resistance.

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“…p53, as an essential tumor suppressor gene, is a guardian of the genome that is the most frequently mutated or deleted in approximately 50% of all human cancers [4][5][6][7]. Activated p53 under stress conditions regulates target gene expression, resulting in the alteration of multiple physiologies including senescence, apoptosis, metabolism, and the cell cycle [8][9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Divergence of the PIERCE1 expression between mice and humans as a p53 target gene

Kim

Lee

et al. 2020

PLoS ONE

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PIERCE1, p53 induced expression 1 in Rb null cells, is a novel p53 target involved in the DNA damage response and cell cycle in mice. These facts prompted us to study the function of PIERCE1 with respect to p53-associated pathophysiology of cancer in humans. Unexpectedly, PIERCE1 did not respond to overexpression and activation of p53 in humans. In this study, we swapped p53 protein expression in human and mouse cells to find the clue of this difference between species. Human p53 expression in mouse cells upregulated PIERCE1 expression, suggesting that p53-responsive elements on the PIERCE1 promoter are crucial, but not the p53 protein itself. Indeed, in silico analyses of PIERCE1 promoters revealed that p53-responsive elements identified in mice are not conserved in humans. Consistently, chromatin immunoprecipitation-sequencing (ChIP-seq) analyses confirmed p53 enrichment against the PIERCE1 promoter region in mice, not in human cells. To complement the p53 study in mice, further promoter analyses suggested that the human PIERCE1 promoter is more similar to guinea pigs, lemurs, and dogs than to rodents. Taken together, our results confirm the differential responsiveness of PIERCE1 expression to p53 due to species differences in PIERCE1 promoters. The results also show partial dissimilarity after p53 induction between mice and humans.

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Effect of EI24 expression on the tumorigenesis of Apc colorectal cancer mouse model

Cited by 3 publications

References 26 publications

miR‑483 promotes the development of colorectal cancer by inhibiting the expression level of EI24

miR‑483 promotes the development of colorectal cancer by inhibiting the expression level of EI24

Intersections of Ubiquitin-Proteosome System and Autophagy in Promoting Growth of Glioblastoma Multiforme: Challenges and Opportunities

Divergence of the PIERCE1 expression between mice and humans as a p53 target gene

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