AZGP1 suppresses the process of colorectal cancer after upregulating FASN expression via mTOR signal pathway

Yu, Wenxiu; Ling, Jun; Yu, Hongbin; Du, Jiang; Liu, Ting

doi:10.4149/gpb_2019061

Cited by 11 publications

(16 citation statements)

References 26 publications

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“… 45 However, another team observed that AZGP1 was highly expressed in colorectal cancer tissue with liver metastasis and associated with unfavorable survival, and that AZGP1 facilitates metastasis by regulating the epithelial-mesenchymal transition. 46 In our study, the expression of AZGP1 was upregulated both in HCT-116-R and CX-1-R cells, suggesting its participation in the acquisition of radioresistance. Subsequently, the microarray data from GEO validated the upregulation of AZGP1 in both radioresistant cells and tissues.…”

Section: Discussionsupporting

confidence: 52%

AZGP1 Up-Regulation is a Potential Target for Andrographolide Reversing Radioresistance of Colorectal Cancer

Fang¹,

Huang²,

Wen³

et al. 2022

PGPM

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Background Radiation resistance is a challenge that limits the therapeutic benefit of colorectal cancer (CRC) treatment, but the mechanism underlying CRC radiation resistance remains unclear. Andrographolide shows a broad-spectrum anti-tumor effect in various malignancies, including CRC, its effect and how it functions in CRC initiation, and radiation have not been established. This study aimed to explore the mechanism of CRC radiation resistance and the potential mechanisms of andrographolide on CRC radiation. Methods Two acquired radioresistant cell lines were established and high throughput sequencing was employed to screen out the differentially expressed genes. The expression of AZGP1, which was upregulated in the acquired radioresistant tissues, was verified by microarray data recomputing. The common targets of andrographolide, CRC initiation, and radiation resistance were obtained, and the corresponding functional enrichment and pathway analysis were performed. The interaction between AZGP1 and andrographolide was investigated using molecular docking. Results AZGP1 was upregulated in both the radioresistant cell model and microarray data. Moreover, AZGP1 was upregulated in cancerous colorectal tissue and displayed a tendency toward elevated expression in patients with an unfavorable prognosis. AZGP1 was identified as the common target of andrographolide, colorectal cancer initiation, and radiotherapy resistance. Ultimately, the protein structure of AZGP1 proved to be closely intertwined with the crystal texture of andrographolide. Conclusion AZGP1 is recognized as a crucial factor for both CRC initiation and radioresistance. Andrographolide may affect the radioresistance of CRC via the targeting of AZGP1. Thus, the combination of andrographolide and AZGP1 intervention might be a promising strategy for improving the treatment benefit of CRC radiotherapy.

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Section: Discussionsupporting

confidence: 52%

AZGP1 Up-Regulation is a Potential Target for Andrographolide Reversing Radioresistance of Colorectal Cancer

Fang¹,

Huang²,

Wen³

et al. 2022

PGPM

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“…The down-regulation of HAGH expression has been shown to have significant antiproliferative effects on colorectal cancer [37]. AZGP1 has been reported to inhibit colorectal cancer progression via the mTOR signaling pathway and has also been shown to suppress the progression of malignant soft-tissue sarcoma cells [38]. LDHD has been reported to be a regulator of energy metabolism and is involved with tumor cell glycolysis within the tumor microenvironment [39].…”

Section: Discussionmentioning

confidence: 99%

Down-regulation of RBP4 indicates a poor prognosis and correlates with immune cell infiltration in hepatocellular carcinoma

Wang

Zhu

et al. 2021

Bioscience Reports

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Recent research has indicated that metabolically related genes play crucial roles in the pathogenesis of hepatocellular carcinoma (HCC). We evaluated the associations between novel biomarkers and retinol-binding protein 4 (RBP4) for predicting clinical HCC outcomes, hub-related genes, pathway regulation, and immune cells infiltration. Bioinformatic analyses based on data from The Cancer Genome Atlas were performed using online analysis tools. RBP4 expression was low in HCC and was also downregulated in pan-cancers compared to normal tissues. RBP4 expression was also significantly different based on age (41–60 years old versus 61–80 years old), and low RBP4 expression levels were associated with advanced tumor stages and grades. Higher RBP4 expression was associated with better overall survival time in HCC patients, and we identified a deletion-mutation rate of 1.4% in RBP4. We also identified ten co-expressed genes most related to RBP4 and explored the relationships between six hub genes (APOB, FGA, FGG, SERPINC1, APOA1, and F2) involved in RBP4 regulation. A pathway enrichment analysis for RBP4 indicated complement and coagulation cascades, metabolic pathways, antibiotic biosynthesis pathways, peroxisome proliferator-activated receptor signaling pathways, and pyruvate metabolism pathways. These results suggest that RBP4 may be a novel biomarker for HCC prognosis, and an indicator of low immune response to the disease.

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“…Loss of AZGP1 can activate the PTEN/Akt and CD44 pathways, thereby promoting metastasis and migration, and it is associated with poor prognosis 19 . Furthermore, AZGP1 overexpression suppresses invasion and cell proliferation by inhibiting MMP‐2 and MMP‐9 expression, and it inhibits the activation of mTOR pathway 38 . Accordingly, loss of AZGP1 promotes EMT, accompanied by increased invasion, decreased apoptosis and proliferation, pro‐survival signals and a shift in energy metabolism 13,20 .…”

Section: Discussionmentioning

confidence: 99%

Degradation of AZGP1 suppresses apoptosis and facilitates cholangiocarcinoma tumorigenesis via TRIM25

Yun,

Jeong,

Kim

et al. 2024

J Cellular Molecular Medi

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Alpha‐2‐Glycoprotein 1, Zinc‐binding (AZGP1, ZAG) is a secreted protein that is synthesized by adipocytes and epithelial cells; it is downregulated in several malignancies such as breast, prostate, liver and lung cancers. However, its function remains unclear in cholangiocarcinoma (CCA). Here, we evaluated the impact AZGP1 in CCA using Gene Expression Omnibus (GEO) and GEPIA. In addition, we analysed AZGP1 expression using quantitative reverse transcription PCR and western blotting. Expression of AZGP1 was nearly deficient in CCA patients and cell lines and was associated with poor prognosis. AZGP1 overexpression upregulated apoptosis markers. Co‐immunoprecipitation experiments showed that AZGP1 interacts with tripartite motif‐containing protein 25 (TRIM25), and tissue microarray and bioinformatic analysis showed that AZGP1 is negatively correlated with TRIM25 expression in CCA. Thereafter, TRIM25 knockdown led to AZGP1 upregulation and induced cancer cell apoptosis. TRIM25 targets AZGP1 for degradation by catalysing its ubiquitination. AZGP1 overexpression significantly suppressed tumour growth in a xenograft mouse model. This study findings suggest that AZGP1 is a potential therapeutic target or a diagnostic biomarker for treating patients with CCA.

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AZGP1 suppresses the process of colorectal cancer after upregulating FASN expression via mTOR signal pathway

Cited by 11 publications

References 26 publications

AZGP1 Up-Regulation is a Potential Target for Andrographolide Reversing Radioresistance of Colorectal Cancer

AZGP1 Up-Regulation is a Potential Target for Andrographolide Reversing Radioresistance of Colorectal Cancer

Down-regulation of RBP4 indicates a poor prognosis and correlates with immune cell infiltration in hepatocellular carcinoma

Degradation of AZGP1 suppresses apoptosis and facilitates cholangiocarcinoma tumorigenesis via TRIM25

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