&lt;p&gt;AOC1 Contributes to Tumor Progression by Promoting the AKT and EMT Pathways in Gastric Cancer&lt;/p&gt;

Xu, Fei; Xu, Yun; Xiong, Ji; Zhang, Jinghui; Wu, Jian; Luo, Jie; Xiong, Jianping

doi:10.2147/cmar.s225229

Cited by 25 publications

(28 citation statements)

References 27 publications

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“…In this study, we found that the mesenchymal hallmarks N-cadherin and vimentin expression decreased in AOC 1-depletion sw480 cells, moreover, the upstream transcription factors SNAIL and Slug were also decreased. Therefore, AOC1 promoted the development of CRC through epithelial-mesenchymal transition, as reported in a previous article ( 8 ). Therefore, targeting AOC1 therapy by reverse the EMT process may be an effective and potential strategy for better prognosis in patients with CRC.…”

Section: Discussionsupporting

confidence: 73%

“…Amine oxidase is mainly involved in tumor growth inhibition and progression (17). Although previous reports revealed that AOC1 affected the occurrence and development of gastric cancer (8) and Wilms tumors (8,18), its role in colorectal cancer has not been elucidated. In this study, we first identified the biological functions of AOC1 in vitro and vivo, especially on proliferation and migration ability.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, a study ( 8 ) revealed that AOC1 promoted the progression of gastric cancer, and another study ( 9 ) has shown that AOC1 was a downstream target gene of the Wilms tumor protein that affected kidney development. However, very little is known about the functions and regulatory mechanisms of AOC1 in CRC.…”

Section: Introductionmentioning

confidence: 99%

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Increased AOC1 Expression Promotes Cancer Progression in Colorectal Cancer

Liu

Tang

et al. 2021

Front. Oncol.

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BackgroundAmine oxidase copper containing 1 (AOC1) is a gene whose biological function in colorectal cancer (CRC) has not been elucidated. Therefore, the purpose of this study was to investigate the clinical significance of AOC1 expression in CRC and its biological function in CRC cell lines.Materials and MethodsAOC1 expression levels were examined in paired CRC and peritumoral tissues, and distant liver metastatic tissues were examined using quantitative real-time PCR, western blotting, and immunohistochemistry staining. The log-rank test and Cox regression model were used to analyze the relationship between AOC1 expression and prognosis. Proliferation assays (Cell Counting Kit‐8 and colony formation assays), migration assays (Transwell and wound healing assays) and xenograft tumor formation in nude mice were performed to assess the biological role of AOC1 in CRC cells.ResultsAOC1 expression significantly increased in human CRC tissues, especially in liver metastases, and was associated with a worse prognosis. In addition, AOC1 had higher expression in tumor organoids than in normal organoids, suggesting that it was highly expressed in the tumor epithelium. Functional analysis demonstrated that AOC1 knockdown inhibited the proliferation and migration of CRC cells by inducing EMT in vitro. Xenograft tumor formation in nude mice showed that knockdown of AOC1 inhibited the tumor xenografts growth in vivo.ConclusionHigh expression of AOC1 was significantly associated with worse clinical outcomes, was an independent risk factor for poor prognosis, and promoted aggressive CRC cell phenotypes. AOC1 is expected to become a novel biomarker for predicting the prognosis of patients with CRC and an effective therapeutic target in clinical practice.

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Section: Discussionsupporting

confidence: 73%

Section: Discussionmentioning

confidence: 99%

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Increased AOC1 Expression Promotes Cancer Progression in Colorectal Cancer

Liu

Tang

et al. 2021

Front. Oncol.

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“…A number of structural and molecular alterations occurs during EMT to produce mesenchymal cells from polarized endothelial cells. In contrast to polarized and static epithelial cells, mesenchymal cells have spindle shape and are not polarized, leading to their migration capability ( Lu et al, 2020 ; Xu et al, 2020 ). The TGF-β is able to enhance invasion and migration of cancer cells via stimulation of EMT ( Li et al, 2019 ).…”

Section: Curcumin and Transforming Growth Factor-beta In Different DImentioning

confidence: 99%

Toward Regulatory Effects of Curcumin on Transforming Growth Factor-Beta Across Different Diseases: A Review

et al. 2020

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Immune response, proliferation, migration and angiogenesis are juts a few of cellular events that are regulated by transforming growth factor-β (TGF-β) in cells. A number of studies have documented that TGF-β undergoes abnormal expression in different diseases, e.g., diabetes, cancer, fibrosis, asthma, arthritis, among others. This has led to great fascination into this signaling pathway and developing agents with modulatory impact on TGF-β. Curcumin, a natural-based compound, is obtained from rhizome and roots of turmeric plant. It has a number of pharmacological activities including antioxidant, anti-inflammatory, anti-tumor, anti-diabetes and so on. Noteworthy, it has been demonstrated that curcumin affects different molecular signaling pathways such as Wnt/β-catenin, Nrf2, AMPK, mitogen-activated protein kinase and so on. In the present review, we evaluate the potential of curcumin in regulation of TGF-β signaling pathway to corelate it with therapeutic impacts of curcumin. By modulation of TGF-β (both upregulation and down-regulation), curcumin ameliorates fibrosis, neurological disorders, liver disease, diabetes and asthma. Besides, curcumin targets TGF-β signaling pathway which is capable of suppressing proliferation of tumor cells and invading cancer cells.

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“…H3K27ac/mC (Fisher’s two-tailed P = 6.5598e-292), H3K4me3/mC (Fisher’s two-tailed P = 3.0205e-273), and H3K4me3/H3K27ac (Fisher’s two-tailed P = 0) were commonly found pairs that were highly significant ( Figure 1B ), and the most frequent triplet marks were H3K4me3/H3K27ac/mC (Fisher’s two-tailed P = 4.8021e-150) and H3K4me1/H3K27ac/mC (Fisher’s two-tailed P = 7.8464e-17). Among genes modified by the six types of epigenetic modifications in Figure 1B , AOC1 was an oncogene in human gastric cancer that activates the AKT signaling pathway ( Xu et al, 2020 ). MYC has been described as a key factor in several human carcinogenic processes ( Calcagno et al, 2008 ).…”

Section: Resultsmentioning

confidence: 99%

Epigenetic Variation Analysis Leads to Biomarker Discovery in Gastric Adenocarcinoma

Zhang

Guo

2020

Front. Genet.

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As one of the most common malignant tumors worldwide, gastric adenocarcinoma (GC) and its prognosis are still poorly understood. Various genetic and epigenetic factors have been indicated in GC carcinogenesis. However, a comprehensive and in-depth investigation of epigenetic alteration in gastric cancer is still missing. In this study, we systematically investigated some key epigenetic features in GC, including DNA methylation and five core histone modifications. Data from The Cancer Genome Atlas Program and other studies (Gene Expression Omnibus) were collected, analyzed, and validated with multivariate statistical analysis methods. The landscape of epi-modifications in gastric cancer was described. Chromatin state transition analysis showed a histone marker shift in gastric cancer genome by employing a Hidden-Markov-Model based approach, indicated that histone marks tend to label different sets of genes in GC compared to control. An additive effect of these epigenetic marks was observed by integrated analysis with gene expression data, suggesting epigenetic modifications may cooperatively regulate gene expression. However, the effect of DNA methylation was found more significant without the presence of the five histone modifications in our study. By constructing a PPI network, key genes to distinguish GC from normal samples were identified, and distinct patterns of oncogenic pathways in GC were revealed. Some of these genes can also serve as potential biomarkers to classify various GC molecular subtypes. Our results provide important insights into the epigenetic regulation in gastric cancer and other cancers in general. This study describes the aberrant epigenetic variation pattern in GC and provides potential direction for epigenetic biomarker discovery.

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<p>AOC1 Contributes to Tumor Progression by Promoting the AKT and EMT Pathways in Gastric Cancer</p>

Cited by 25 publications

References 27 publications

Increased AOC1 Expression Promotes Cancer Progression in Colorectal Cancer

Increased AOC1 Expression Promotes Cancer Progression in Colorectal Cancer

Toward Regulatory Effects of Curcumin on Transforming Growth Factor-Beta Across Different Diseases: A Review

Epigenetic Variation Analysis Leads to Biomarker Discovery in Gastric Adenocarcinoma

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